Seminars

Speaker

:

Dr. Kshitij Jadhav

Affiliation

:

University of Cambridge

Venue

:

Video Conference

Time

:

04.00 PM

Date

:

28 Jun 2022

Abstract

:

Normative development in adolescence indicates that the prefrontal cortex is still under development thereby unable to exert efficient top-down inhibitory control on subcortical regions such as the basolateral amygdala and the nucleus accumbens. This imbalance in the developmental trajectory between cortical and subcortical regions is implicated in expression of the prototypical impulsive, compulsive, reward seeking and risk-taking adolescent behavior. Here, I demonstrate that a chronic mild unpredictable stress procedure during adolescence in male Wistar rats affects normal behavioral maturation such that they continue to express adolescent-like impulsive, hyperactive, and compulsive behaviors into late adulthood. This behavioral affliction is associated with the hypoexcitability of prelimbic cortex (PLC) pyramidal neurons and reduced PLC-mediated synaptic glutamatergic control of BLA and nucleus accumbens core (NAcC) neurons that lasts late into adulthood. At the same time stress exposure in adolescence results in the hyperexcitability of the BLA pyramidal neurons sending stronger glutamatergic projections to the NAcC. Chemogenetic reversal of the PLC hypoexcitability decreased expression of compulsive behavior in rats exposed to stress during adolescence, suggesting a causal role for PLC hypoexcitability in this stress-induced behavioral expression.

Speaker Bio

:

Dr. Kshitij Jadhav is currently a postdoctoral neuroscientist working at the University of Cambridge, UK. He completed his medical school training (MBBS) from Mumbai during when he developed a keen interest in psychiatry. In a bid to explore psychiatric disorders from a pharmacological perspective he pursued MD Pharmacology from Mumbai. On receiving the highly competitive Swiss Government Excellence Fellowship, Dr. Kshitij moved to University of Lausanne, Switzerland to pursue fundamental research and focused on adolescent stress and its long-term behavioral effects. To explore the neurocircuitry adaptations of adolescent stress exposure, he applied and received the competitive Doc mobility Fellowship from Swiss National Science Foundation (SNSF) which allowed him to pursue slice electrophysiology at National Institute on Drug Abuse – NIH at Baltimore, USA in his final year of PhD. He defended his thesis titled ‘Stress Deceleration Theory’ in October 2019 which was awarded the ‘Best Thesis Award’ from Societie Academique Vaudoise making him the first Neuroscience graduate to receive this award (https://www2.unil.ch/diesacademicus-2020/kshitij-jadhav/index.html). He then received an Early Postdoc Mobility fellowship from SNSF to continue his postdoctoral research at Cambridge. He possesses a unique blend of expertise right from being a clinician, to a fundamental neuroscientist as well as the use of machine learning techniques with behavioral neuroscience.

Speaker

:

Dr. Latika Nagpal

Affiliation

:

Research Associate , Howard Hughes Medical Institute (HHMI)
PhD, Department of Biotechnology, University of Calcutta

Venue

:

Video Conference

Time

:

04.00 PM

Date

:

22 Apr 2022

Abstract

:

My doctoral thesis was on ‘Study of Novel Pyrimidine Imidazole Derivatives as Inducible Nitric Oxide Synthase Inhibitors’ from the Department of Biotechnology, University of Calcutta, India and Cleveland Clinic Lerner Research Institute under the supervision of Prof(s) Koustubh Panda and Dennis Stuehr. I would present my graduate research on understanding the structure-function based catalytic properties of nitric-oxide synthase (NOS) and its possible intervention by suitable non-toxic and NOS-specific compounds for the clinical management of diseases associated with dysfunctional expression of iNOS. We developed two non-toxic, highly-specific novel pyrimidine imidazole inhibitors against iNOS through Quantitative Structure Activity Relationship (QSAR) analysis and studied the mechanism of their action both in in-vitro and ex-vivo models of iNOS over-expression. As a sequel to this work, we developed a novel in-vivo probe for elucidating the possible causal role of iNOS in diseases implicated with its abnormal expression which includes diabetes, cardiovascular diseases, inflammatory diseases like emphysema and asthma as well as neurodegenerative diseases like Parkinson, Alzheimer’s etc.

My postdoctoral research in the lab of Prof. Solomon H. Snyder at the Department of Neuroscience, Johns Hopkins University School of Medicine was to unravel the functional role of inositol hexakisphosphate kinases in the brain. I identified the key binding partner for IP6K2, 4.1N. This protein was discovered to be a novel and selective partner for IP6K2. This work established a role of IP6K2 in granule cells regulating Purkinje cells and locomotor functions via 4.1N. My subsequent postdoctoral research was focused on elucidating the role of another interactor for IP6K2, namely Creatine Kinase-B (CK-B). We found a novel role for IP6K2–CK-B regulating oxidative stress and mitochondrial functions. This project involved studying the mechanism of abrogation of IP6K2-CK-B interaction leading to synaptic loss, mitochondrial dysfunction as well as neurodegeneration. Given my background in studying the mechanism of various diseases caused by nitrosative and oxidative stress, I would like to explore the redox mechanisms governing neurodegenerative diseases mainly Brain Ischemia and Alzheimer’s disease.

Speaker Bio

:

Speaker

:

Dr. Sriparna Ghosal

Affiliation

:

Venue

:

Video Conference

Time

:

04.00 PM

Date

:

18 Feb 2022

Abstract

:

The organismal stress response is an integrated physiological and behavioral state to actual or perceived threat to homeostasis. In this presentation, I will discuss the compendium of results about cortical and subcortical mechanisms contributing to the coordination of whole-body stress reactivity. Next, I will present how reorganization of prefrontal cortical stress-control circuitry in the chronically stressed brain contributes to depression, and how this relates to rapid acting antidepressant such as the NMDA receptor antagonist ketamine or scopolamine, a non-selective muscarinic acetylcholine receptor antagonist. Finally, I will describe on neurobiological and mitochondrial bases of individual differences in stress responsiveness, close with the role of mitochondrial functions in specific cell-types in controlling stress-related psychopathologies such as, depression.

Speaker Bio

:

Speaker

:

Sathya Puthanveettil

Affiliation

:

PhD,
Department of Neuroscience,
Scripps Florida, Jupiter, FL 33458. USA

Venue

:

Video Conference

Time

:

04.00 PM

Date

:

18 Jan 2022

Abstract

:

Decades of research on the molecular and cellular mechanisms underlying long-term memory storage (LTM) have established the requirement of changes in the expression of specific genes and synthesis of new proteins in dendrites.  These changes ultimately result in the remodeling of synaptic connections and formation of new ones. My lab studies how the nuclear and synaptic changes are coordinated by assessing the regulation and function of molecular motor proteins that mediate the active transport of proteins, RNAs and organelles along the microtubule cytoskeleton, and their cargo complexes. In this discussion, I will focus on the role of Kinesin family of motor proteins (KIFs) that mediate the active transport from the cell body to dendrites. Specifically, the diversity of KIFs and their cargos in modulating synapse function, structural plasticity and LTM will be discussed. Further, I will highlight the significance of KIFs in developing novel neurotherapeutics.

Speaker Bio

:

Speaker

:

Vijendra Sharma

Affiliation

:

Ph.D. Research Associate,
Department of Biochemistry,
McGill University, Canada.

Venue

:

Video Conference

Time

:

05:00 PM

Date

:

30 Aug 2021

Abstract

:

Translational control of gene expression is a dynamically regulated process essential for higher cognitive functions. The brain’s general and transcript-specific translation rates are determined by the level and activity of the components of the eukaryotic initiation factor 2 ternary complex (eIF2-TC) and eIF4F complex (composed of eIF4E, eIF4G, and eIF4A). Diverse stress stimuli activate the integrated stress response (ISR) pathway via phosphorylation of the alpha (α) subunit of eIF2 (p-eIF2α), thereby inhibiting general protein synthesis but stimulating the translation of specific mRNAs with upstream open reading frames in their 5′UTRs to cope with the stress. Conversely, the genetic and pharmacological inhibition of ISR kinases or mimicking reduced p-eIF2α with the ISR inhibitor ISRIB or mutating the eIF2α phosphorylation site (serine 51) enhances long-term memory. Our advanced genetic mouse models of eIF2, combined with gene discovery studies, allowed us to dissect the cell-types-specific mechanisms and neuronal circuits by which the ISR pathway gates cognitive processing in the brain. The additional major pathway modulating translation initiation is the mammalian target of rapamycin complex 1 (mTORC1), which integrates multiple signaling pathways to control translation initiation by phosphorylating eukaryotic initiation factor (eIF4E) binding proteins (4E-BP1 and 4E-BP2), a negative regulator of protein synthesis that functions by sequestering the cap-binding subunit of eIF4F (eIF4E). Using transgenic mouse lines lacking 4E-BP2 in different neuronal types, we identified a subset of inhibitory interneurons in which increased mTORC1-dependent translation promotes epileptogenesis. These studies provide mechanistic insights into the role of translational control in regulating neuronal functions and might facilitate the development of therapies to alleviate brain disorders such as epilepsy and neurodegenerative conditions associated with memory loss.

Speaker Bio

:

Speaker

:

Dr. Sufyan ashhad

Affiliation

:

Dept Of Neurobiology, UCLA.

Venue

:

Video Conference

Time

:

05:00 PM

Date

:

25 Aug 2021

Abstract

:

Mammalian breathing is robust, virtually continuous throughout life, and yet is exceptionally labile to i) respond rapidly to increases in metabolic demands for oxygen, e.g., fleeing a predator or chasing prey; ii) change pattern for essential reflexes, e.g., cough, sigh; and sync with non-ventilatory behaviors, e.g., vocalization, swallowing. The neuroanatomical core of the breathing circuit is the preBötzinger Complex (preBötC) located in the brainstem. However, decades after its discovery, the mechanisms underlying the generation and control of breathing patterns remain elusive. In this talk, I will present evidence from experimental and computational studies that reveal that the inspiratory activity in every breath cycle is generated by spike-synchronization of rhythmogenic preBötC neurons. This synchronization is gated by the excitation-inhibition balance in the preBötC network that modulates its rhythmicity. Furthermore, the preBötC inspiratory burst generation is an all-or-none phenomenon –a manifestation of attractor dynamics in neuronal networks. I will show that such dynamics impart robustness to the breathing rhythm while allowing for the necessary flexibility to respond to external inputs that coordinate breathing with behaviors such as chewing, swallowing, phonation, and the emotional and cognitive control of breathing. The robustness and lability of the preBötC network are effectuated by a fat-tailed synaptic strength distribution, as observed in the network models constructed from experimentally derived neuronal and network parameters. Such connectivity strategy in this vital rhythmogenic network augments neuronal synchronization and attractor dynamics through coincident convergent inputs, contributing to its reliability and responsiveness. These analyses reveal that the fat-tailed synaptic strength distribution, observed in several brain regions, provides a unified mechanism to balance the contrasting requirements underlying input sensitivity and response reliability for vital microcircuit operations. Understanding neuronal and network mechanisms underlying the preBötC attractor dynamics is crucial to study widespread pathologies caused by breathing malfunction and explore their solutions.

Speaker Bio

:

Speaker

:

Dr. Nandkishore Prakash

Affiliation

:

University of California San Diego.

Venue

:

CNS Ground Floor Seminar Hal

Time

:

04:00 PM

Date

:

10 Mar 2020

Abstract

:

Depression and other mental disorders can be induced by chronic or traumatic stressors. However, some individuals (humans as well as animal models) are resilient and do not develop depression in response to chronic stress. A complete picture of the differences between susceptible and resilient individuals is necessary to understand how the plasticity of limbic circuits is associated with the pathophysiology of stress-related disorders. Our study identifies a novel molecular marker of susceptibility to stress-induced anhedonia, a core symptom of depression, and a means to modulate it.

Stress-induced anhedonia was assessed in adult male rats using social defeat and intracranial self-stimulation (ICSS), while changes in serotonergic phenotype were investigated using immunohistochemistry and in situ hybridization. Susceptible, but not resilient, rats displayed an increased number of neurons expressing the biosynthetic enzyme for serotonin, tryptophan-hydroxylase-2 (TPH2), in the ventral subnucleus of the dorsal raphe (DRv). Further, a decrease in the number of DRv glutamatergic neurons was observed in all stressed animals. This neurotransmitter plasticity is dependent on DR activity, as chemogenetic activation of amygdala corticotropin-releasing hormone (CRH)+ neurons abolished the increase in DRv TPH2+ neurons and ameliorated stress-induced anhedonia in susceptible animals. These findings uncover a molecular signature of vulnerability to stress-induced anhedonia and the active nature of resilience. Further investigation into cellular and circuit mechanisms of resilience, will guide the development of new treatments for depression.

Speaker Bio

:

Speaker

:

Dr. Niranjan Kambi

Affiliation

:

University of Wisconsin-Madison.

Venue

:

CNS Ground Floor Seminar Hall

Time

:

12:00 PM

Date

:

20 Feb 2020

Abstract

:

Episodic memory refers to our unique ability to record and reconstruct our past experiences. Previous studies have shown that the hippocampus, retrosplenial cortex (RSC) and anterior thalamus (AT) form prominent nodes of an interconnected brain circuit responsible for episodic memory. However, the exact nature of their role and the mutual interactions for memory processing is unknown. To address these questions, I simultaneously recorded spikes and local field potentials (LFP) from the AT, hippocampus and RSC of two macaques performing a novel visuospatial scene memory task. We used diffusion MRI to target linear microelectrode arrays to interconnected sites of this hippocampo-thalamo-cortical network, and structural MRI of electrodes in situ to confirm electrode positions.

I will talk about the preliminary analysis from the spiking activity in these brain regions during mnemonic processing of scenes. These results suggest that spiking in RSC and ATN represent spatial and temporal aspects of the scenes. Further, I will also show initial results of dynamic interactions between these brain regions in the service of memory. Overall, this study suggests an important role for the anterior thalamus and retrosplenial cortex in the extended hippocampal system supporting episodic memory.

If time permits, I will also talk about other projects in the lab I worked on and my vision in the future regarding how to proceed further in the investigation of the neural basis of memory.

Speaker Bio

:

Speaker

:

Dr. Naveen Sendhilnathan

Affiliation

:

Columbia University.

Venue

:

CNS Seminar Hall Ground Floor

Time

:

04:00 PM

Date

:

14 Feb 2020

Abstract

:

Speaker Bio

:

Speaker

:

Dr. David Perrais

Affiliation

:

Interdisciplinary Institute of Neuroscience, CNRS and University of Bordeaux, France

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

11:00 AM

Date

:

28 Jan 2020

Abstract

:

Endocytosis and recycling in neuronal dendrites play a critical role in synaptic function and plasticity. We have used live cell fluorescence imaging to visualize individual exocytic and endocytic events in cultured hippocampal neurons with high temporal resolution. First, we show that clathrin-coated endocytic zones (EZs) are optically static in mature neurons and that they are slightly enriched towards synapses. A pH exchange protocol reveals that these stable EZs produce endocytic vesicles containing the cargo transferrin receptor (TfR) continuously. These structures are slightly enriched near synapses. Perisynaptic EZs represent preferential sites for the endocytosis of postsynaptic AMPA-type receptors (AMPARs), but not for non-synaptic TfRs. Moreover, the frequency of AMPAR endocytosis events increases after the induction of NMDAR-dependent chemical LTD, but the activity of perisynaptic EZs is not differentially regulated. Second, we recorded exocytosis events of recycling endosomes (REs). We found that exocytosis events are grouped into two categories: short burst events where receptors diffuse into the plasma membrane in a few seconds, and long display events where receptors remain visible and clustered after exocytosis for many seconds. Using two color imaging and fast extracellular solution changes, we show that display events correspond to the transient opening of a fusion pore (“kiss-and-run”) with a median opening time of 2.6 s which restricts the diffusion of multiple receptor types and bound cargo. Moreover, the RE marker Rab11 remains enriched after display exocytosis events, and controls the mode of RE exocytosis. We are currently characterizing some of the molecular players of RE exocytosis and its modulation during synaptic plasticity.

References:
Jullié D, Choquet D, Perrais D (2014) Recycling Endosomes Undergo Rapid Closure of a Fusion Pore on Exocytosis in Neuronal Dendrites. J Neurosci 34:11106–11118.

Martineau M, Somasundaram A, Grimm JB, Gruber TD, Choquet D, Taraska JW, Lavis LD, Perrais D (2017) Semisynthetic fluorescent pH sensors for imaging exocytosis and endocytosis. Nat Commun 8:1412.

Rosendale M, Jullié D, Choquet D, Perrais D (2017) Spatial and Temporal Regulation of Receptor Endocytosis in Neuronal Dendrites Revealed by Imaging of Single Vesicle Formation. Cell Rep 18:1840–1847.

Rosendale M, Van TNN, Grillo-Bosch D, Sposini S, Claverie L, Gauthereau I, Claverol S, Choquet D, Sainlos M, Perrais D (2019) Functional recruitment of dynamin requires multimeric interactions for efficient endocytosis. Nat Commun 10:4462.

Speaker Bio

:

Speaker

:

Dr. Achira Roy

Affiliation

:

Seattle Children’s Research Institute, USA.

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

28 Jan 2020

Abstract

:

Mammalian development involves complicated cell morphogenesis and interactions between transcription factors and signaling molecules. The PI3K-AKT-MTOR pathway is one such central intracellular signaling pathway, crucial for cell growth and metabolism. Activating mutations in this pathway have long been linked to cancer. Strongly activating PI3K mutations, found most commonly in cancer, also result in severe brain overgrowth and dysplasia; and can often cause intellectual disabilities, autism, hydrocephalus and intractable epilepsy.

I will present my postdoctoral work that identified basic cellular mechanisms and critical developmental periods behind PI3K-related brain overgrowth and dysplasia in conditional mouse mutants. In addition, I will discuss new small-molecule drug therapies that suppressed seizure, cortical dysplasia and developmental hydrocephalus in our models, thus creating promising new therapeutic avenues for such comorbidities.

Speaker Bio

:

Speaker

:

Dr. Ruadhan O'Flanagan

Affiliation

:

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

24 Jan 2020

Abstract

:

The spike of an individual neuron signals the truth of a corresponding logical proposition, and a pattern of these spikes in a single region of the brain become bound together into a single data structure that can be referenced and regenerated from elsewhere in the brain when an oscillation such as the gamma rhythm can escort that spiking activity around a loop that returns it to its original region and reliably regenerates the same pattern of spikes. The circulation of rhythms around neural circuits stabilize these recurrent patterns of activity through spike-timing-dependent plasticity, which allows patterns encountered in experience to be recognized and recalled at later times. This phenomenon is nearly universal within the brain: For example, an image can be recalled starting from a concept by circulating spikes around a loop connecting visual and prefrontal cortex or the same conceptualization can reliably be reactivated upon recognition of a familiar image. In the hippocampus and the entorhinal cortex, multiple oscillatory rhythms, and symbolic data representations interact in a specific way that connects data representations spatiotemporally and makes navigation possible.

Speaker Bio

:

Speaker

:

Prof. Jesús Malo

Affiliation

:

Professor of Vision Science,
Department of Optics Universitat de València,
Spain.

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

11:30 AM

Date

:

14 Jan 2020

Abstract

:

When the visual environment is suddenly changed, some textures may fade out, static objects seem to move, and colors change their hue. These visual illusions described in humans long ago have been recently reported for artificial neural networks too. In this talk, I analyze why this is the case. On the one hand, illusions in humans are explained as a by-product of our adaptation to the PDF of the visual environment. In particular, multivariate equalization strategies induce operation regimes that explain illusions while the system readapts to the new environment [1]. The emergence of human-like nonlinear responses and illusions from infomax goals is consistent with the good information-theoretic performance of psychophysically-tuned networks [2-4].

On the other hand, I show that brightness and color illusions arise in artificial neural networks trained to solve low-level vision tasks (e.g. denoising and deblurring) [5]. We not only look at the arguable (artificial) physiological response of the networks, but we also study the artificial psychophysics (e.g. asymetric color matching), which is directly comparable with human behavior [6]. We find out that illusions appear because the artificial networks develop filter functions that are similar to our Contrast Sensitivity Functions in opponent chromatic channels, in agreement with Wiener-like regularization and the statistics of natural images [6]. Interestingly, if the structure of the network is too deep and too specific for the denoising problem, the visual illusions disappear. Finally, I will discuss the synthesis of visual illusions in a Generative Adversarial Network (GAN) framework [7]. Again, the role of vision models in the discriminating network and the description of image statistics is the key to generate non-trivial illusions in GANs.

In conclusion, the adaptation of a perceptual system to the statistics of the signal leads to illusions in unusual or dynamic environments either the system is biological or artificial.

References:

[1] Laparra, V. and Malo, J. (2015) “Visual aftereffects and sensory nonlinearities from a single statistical framework” Front. Hum. Neurosci., https://doi.org/10.3389/fnhum.2015.00557

[2] Malo, J. and Laparra, V. (2010) “Psychophysically-tuned Divisive Normalization factorizes the PDF of natural images” Neural Computation, Vol. 22, 12:3179-3206 https://isp.uv.es/papers/Malo_Laparra_Neural_10b.pdf

[3] A. Gómez-Villa, M. Bertalmío, J. Malo (2019) “Visual Information Flow in Wilson-Cowan networks” Accepted in J. Neurophysiol. Preprint in https://arxiv.org/abs/1907.13046

[4]  Malo, J. (2019) Spatio-Chromatic Information available from different Neural Layers via Gaussianization. https://arxiv.org/abs/1910.01559

[5] Gomez-Villa, A., et al. (2018) “Convolutional Neural Networks Can Be Deceived by Visual Illusions“. Proc. IEEE Conf. Comp. Vision Patt. Recog. CVPR18, Prerpint in https://arxiv.org/abs/1811.10565

[6] Gomez-Villa, Martin, Vazquez, Bertalmio, & Malo, J., (2019) “Visual Illusions also deceive Convolutional Neural Networks: Analysis and Implications”. https://arxiv.org/abs/1912.01643

[7] Gomez-Villa, Martin, Vazquez, Bertalmio, & Malo, J., (2019) “Synthesizing Visual Illusions Using Generative Adversarial Networks” https://arxiv.org/abs/1911.09599

Speaker Bio

:

Jesús Malo (1970) received the Ph.D. degree in Physics in 1999 from the Universitat de València for his work on Computational Visual Neuroscience with applications to Image Processing. He was the recipient of the Vistakon European Research Award in 1994 for his experimental work in Physiological Optics. In 2000 and 2001 he worked as Fulbright Postdoc at the Vision Group of the NASA Ames Research Center (with A.B. Watson), and as Visiting Researcher at the Lab of Computational Vision of the Center for Neural Science, New York University (with E.P. Simoncelli) in 2001 and 2013. Currently, he is a Full Professor of Vision Science at the Dept. of Optics of the Universitat de València, and he leads the research on Visual Neuroscience at the Image and Signal Processing Group of the Universitat de València. He has been Associate Editor of IEEE Trans. I’m. Proc. (2009-2013) and now he is Academic Editor of PLOS ONE, Associate Editor of Frontiers in Neuroscience (specialty Perception Science). He is interested in models of low-level human vision, their relations with information theory and statistical learning, and their applications to image processing and vision science experimentation.

For more information
https://scholar.google.com/citations?user=0pgrklEAAAAJ&hl=en
https://isp.uv.es/excathedra.html

Speaker

:

Sridevi Venkatesan

Affiliation

:

Ph.D. candidate,
Department of Physiology,
The University of Toronto.

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

8 Jan 2020

Abstract

:

Cholinergic neuromodulation of the prefrontal cortex (PFC) is important for top-down control of attention. Layer 6 pyramidal neurons in the PFC express the α5 nicotinic acetylcholine receptor subunit encoded by Chrna5 which is critical for performing demanding attention tasks. However, mechanisms by which the α5 subunit influences endogenous cholinergic signaling in the PFC are unclear. Here we use whole-cell electrophysiology to investigate the role of the α5 subunit in response to a physiologically relevant stimulus pattern of optogenetic acetylcholine (ACh) release in brain slices. The findings in male and female mice demonstrate that the α5 subunit is critical for achieving an initial rapid response to ACh release. Neurons lacking the α5 subunit exhibit a sluggish cholinergic response with significantly slower rise and prolonged decay. In both genotypes, the prefrontal cholinergic release appears to be regulated by muscarinic M2 receptors. After blockade of this auto-inhibition, it is clear that only the timing but not the magnitude of the inward current in response to brief stimulation is compromised in α5 knockouts. Under conditions of sustained acetylcholine or acute nicotine exposure however, the α5 subunit becomes critical for protecting the endogenous cholinergic signaling from desensitization. Taken together, this work demonstrates that the α5 subunit is necessary for generating the rapid onset of postsynaptic cholinergic excitation considered important for cognition and for allowing this response to continue when challenging or stressful conditions greatly elevate prefrontal acetylcholine levels.

Speaker Bio

:

Speaker

:

Dr. Kshitij S. Jadhav

Affiliation

:

MBBS, MD (Pharmacology),
Ph.D. (Neuroscience)

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

10:00 AM

Date

:

7 Jan 2020

Abstract

:

Adolescence, defined as a transition phase towards autonomy and independence, is considered a natural time of learning and adjustment, particularly in the setting of long-¬‐term goals and personal aspirations. The development of self-¬‐regulatory competences is a normative process, that depends on brain maturation and social as well as environmental influences, at the end of which young adults have acquired the aptitude to better regulate their emotions and impulsivity. Brain development during this critical period of life can be influenced by several factors, especially stress.In the present experimentsadolescent Wistar male rats were subjected to chronic mild unpredictable stress (CMUS) for 3 consecutive weeks starting from the post-¬‐weaning phase (P21-¬‐P42). Behavioural, these rats display increased disinhibited, hyperactive, impulsive, inattentive and reward-seeking behaviors. Interestingly these behaviors persist well into late adulthood indicating that these behavioral changes induced by exposure to stress during adolescence are long-¬‐lasting. Exposure to stress during adolescence also resultedinhyper-¬‐excitable Basolateral amygdala andhypo-¬‐excitable Prelimbic cortex pyramidal neurons evaluated using ex-¬‐vivo slice patch clamp electrophysiology. These electrophysiological characteristics persisted at both P50 andP90 indicating long-¬‐term, possibly irreversible, changes. Furtherevidence collected by patch clamp ex-¬‐vivo electrophysiology and optogenetic techniques using channelrhodopsin indicated that the stress exposure during adolescence resulted ina weakerglutamatergic projection and by extension lower control of the Prelimbic cortex over nucleus accumbens core as well as the basolateral amygdala. This indicates a weaker top-¬‐down control from the prefrontal cortex to the subcortical regions due to stress exposure during adolescence. Using the same technique, we show that the basolateral amygdala demonstrate-stronger glutamatergic projections to the nucleus accumbens core and weakerglutamatergic projections from the basolateral amygdala to the prelimbic cortex. Importantly, all behaviors displayed by theratsundergoing the CMUS procedure in adolescence are reminiscent of oftypical adolescent behavior but displayed by them well into late adulthood. Also, all the electrophysiological evidence indicates that adolescent patterns of brain circuitry stay put well into late adulthood after exposure to stress during adolescence. Together, we propose the following: ‘Stress deceleration theory: Chronic stress in adolescence results in arrested development of brain circuitry patterns and behaviors, preventing the development of adult‐like behaviors and strategies.

Speaker Bio

:

Speaker

:

Rajat Saxena

Affiliation

:

Graduate student,
The University of California,
Irvine.

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

24 Dec 2019

Abstract

:

The ability to extract abstract knowledge from experience is a defining property of high-level cognition and intelligence. Early theories suggested that this extraction takes place in the neocortex (NC), using episodic memory information stored in the hippocampus (HC). Thus, there is a need for NC circuits to encode two principal types of information: (1) a global context in which experiences occur (‘index’), and (2) the attributes of the experiences themselves (the ‘content’), which are encoded in a relatively context-free manner and may include representations of categories and schemas. We suggest a broad generalization that context is represented predominantly in superficial NC (LII-III) whereas content (i.e., the attributes of episodes and the categories and schemas derived therefrom) are encoded predominantly in deep layers (LV-VI). Together, the superficial and deep layers comprise a rapidly modifiable, heteroassociative circuit that enables the global index code for memory to retrieve the corresponding locally encoded attributes and schemas. Using a combination of 2-photon imaging and multisite silicon probe recording, I will demonstrate how contextual information (‘index’) from the HC is transferred to the superficial NC (RSC, PPC, V1, M1, S1), which are the main recipients of HC return projections. Finally, I will present work based on deep linear neural networks trained on data from hierarchically structured environments to gain new insights into when the integration of new information in the cortex-like network is fast or slow and how integration might be made more efficient.

Speaker Bio

:

Speaker

:

Dr. Abhishek Banerjee

Affiliation

:

D.Phil, Associate Professor in Systems Neuroscience, Institute of Neuroscience, Newcastle University Medical School.

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

17 Dec 2019

Abstract

:

Decision-making involves multiple cognitive maps across distributed brain areas. It is less clear how changes in neuronal responses re-maps during flexible behaviour in animals. In this talk, I will highlight one such neurobiological mechanism in the orbitofrontal cortex, a key frontal cortical structure for reward-based decisions. Based on these findings, I will also propose a new conceptual framework based on computational psychiatry to understand pathophysiology in complex neurological brain disorders such as OCD and autism spectrum disorders.

Speaker Bio

:

Speaker

:

Dr. Dushan N. Wadduwage

Affiliation

:

Research Fellow,
Harvard University.

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

21 Nov 2019

Abstract

:

Most excitatory synapses in the mammalian brain are located on dendritic spines, making spines convenient proxies for excitatory synaptic presence. When in-vivo two-photon imaging revealed that dendritic spines are dynamic structures, their addition and elimination were, interpreted as excitatory synapse gain and loss. Currently, imaging a full L2/3 dendritic arbor at synaptic resolution with a standard point scanning two-photon microscope (PS-TPM) takes 60-90 minutes. Imaging rapid synaptic remodeling events on the order of minutes, across a large volume, is thus not possible. To enable imaging rapid dynamic events of this nature, through scattering tissue, we are now developing a range of wide-field multi photon microscopy technologies. The imaging methods are based on two key techniques; temporal focusing, and computational imaging. We use temporal focusing for depth selective multiphoton excitation in wide-field. Excitation light, at NIR wavelengths, penetrates deep; the emission photons, at visible wavelengths, however, encounter severe scattering. We use computational imaging to de-scatter these photons with a technique we call De-scattering with Excitation Patterning or DEEP. We demonstrate DEEP with classical computational imaging algorithms as well as state-of-the-art deep convolutional neural networks. Our results suggest orders of magnitude faster imaging speeds, that could potentially render, neuroscience experiments that were previously prohibitively slow, possible.

Keywords: DEEP-TFM, Temporal focusing, Two-photon microscopy, Computational imaging

Speaker Bio

:

Speaker

:

Dr. John Jeka

Affiliation

:

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

5 Nov 2019

Abstract

:

The evolutionary development of bipedal stance, which freed the hands from locomotion, is considered the fundamental distinction between humans and our closest relatives. Accompanying that development is the problem of stability. Engineered devices, such as cars and robots, solve the stability problem by having a wide base of support and/or concentrating the bulk of its weight lower down. However, the human body has evolved with more than just upright stability as a constraint, with its mass concentrated higher up in the trunk, making it inherently unstable and prone to falls. This “mechanically unstable” design has been matched with a sophisticated control system to maintain upright stance during functional behavior (e.g., tool-use), lending itself to many fundamental questions about how the nervous system solves this complex control problem. Moreover, the neural and biomechanical subsystems that enable standing are subject to injury and dysfunction, leading to many disease populations with limited options based upon current medical treatments. My research group aims to bridge the basic and applied science underlying balance control. Combined with techniques that precisely manipulate input from visual, vestibular and proprioceptive sensory systems, postural control mechanisms are studied with particular regard for the processes involved in fusing information from different sensory systems to provide an overall estimate of body dynamics. Computational methods combine mechanisms of multisensory fusion with biomechanical investigations of multilink body dynamics to develop realistic models of human postural control. The combination of experimental studies with computational models are then applied to the development of new techniques and assistive devices for treatment of patient populations with balance disorders including individuals with the loss of inner ear (vestibular) function, fall-prone older adults and Traumatic Brain Injury.

Speaker Bio

:

Dr. Jeka was an NIMH predoctoral fellow and received his PhD in Neuroscience from Florida Atlantic University. He then received an NIH NRSA postdoctoral fellowship with the Ashton Graybiel Spatial Orientation laboratory at Brandeis University. After 18 years at the University of Maryland – College Park, he moved to Temple University as Professor and Chair of the Department of Kinesiology from 2013-2017 and is currently Chair of Kinesiology & Applied Physiology at the University of Delaware. His research interests include multisensory fusion for the control of human postural/locomotion and its application to the rehabilitation of individuals with balance disorders including cerebral palsy, vestibular loss and traumatic brain injury. He has received over $10 million in funding from the NIH, NSF, NASA and private sources such as the Erickson Foundation and the Shriners Foundation. He currently has two patents pending and is the Chief Scientific Officer of Treadsense, Inc., which develops technology for enhanced mobility.

Speaker

:

Dr. Ravi Muddashetty

Affiliation

:

inStem

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

9 Jul 2019

Abstract

:

Problems associated with protein synthesis are at the core of many synaptic dysfunctions. But the path to understanding the mechanism of this process is full of twists and turns and this quest has taken us from synaptic compartments to all the way to the nucleus and nucleolus. In the current talk, I will discuss two aspects of this effort and the outcome. Synaptic activity leads to the synthesis of many proteins with a huge impact on plasticity. An important aspect of protein synthesis is that it is energetically expensive and hence it is imperative to consider bioenergetics in the context of synaptic translation. Our work shows that AMP kinase (AMPK), a key regulator of energy metabolism also plays a critical role in determining the NMDAR and mGluR mediated translation at the synapse. This indicates a synergy and balance between energy metabolism and translation. Any perturbation to this delicate balance may lead to synaptic defects. In our quest to understand the molecular mechanism of synaptic signaling, we have identified many different classes of RNA molecules having a critical role in regulating activity mediated translation. We propose that these different classes of RNAs along with specialized RBPs such as FMRP integrate the activity mediated translation in neurons to facilitate synaptic plasticity. These mechanisms will provide new insight into the role of translation defects contributing to neurodevelopment and neurodegenerative disorders.

Speaker Bio

:

Speaker

:

Dr. Abhishek Bhattacharya

Affiliation

:

Columbia University

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

3 Jul 2019

Abstract

:

Understanding the synaptic wiring of an entire nervous system – its ‘connectome’ – is an essential first step to elucidate how the nervous system processes information and generates behavior. Connectomes have two components – the wiring diagram of all chemical synapses and that of all electrical synapses. My work focuses particularly on the electrical synaptic wiring, which has generally remained the stepchild of synapse biology, particularly in regards to its development and plasticity. My work is a first ever attempt to understand the molecular logic of electrical synaptic specificity and functional diversity of an entire nervous system, which has been proposed to be defined by the neuron-specific complement of electrical synapse constituents. I systematically defined the molecular composition of the electrical connectome of the nematode C. elegans through a genome- and nervous-system-wide analysis of the expression patterns of the invertebrate electrical synapse constituents, the innexins. I observed highly complex combinatorial expression patterns throughout the nervous system. This work provides insights into the yet unknown molecular determinants of the electrical synaptic specificity and functional diversity and provides novel entry points to decipher them. I will also present my work showing that these innexin expression patterns change in a strikingly Neuron-type-specific manner throughout the nervous system when animals enter a diapause arrest stage under harsh environmental conditions. I found an intersectional gene regulatory mechanism that mediates dynamic innexin expression plasticity in a neuron-type- and environment-specific manner, which ultimately leads to circuit plasticity. By analyzing individual synapses, I demonstrated that these stage-specific electrical synapse remodelings are responsible for particular aspects of the stage-specific behavioral alteration.

Speaker Bio

:

Speaker

:

Prof. Mayank Mehta

Affiliation

:

Department Of Physics, UCLA

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

20 Jun 2019

Abstract

:

Cortical δ rhythm was discovered in the 1920s. Hippocampal θ rhythm was discovered in 1956. Since then β and γ rhythms have been discovered too. How do these rhythms arise and how do they influence neural responses? I will discuss some of these issues and the discovery of new brain rhythm.

Speaker Bio

:

Speaker

:

Prof. GAITI HASAN

Affiliation

:

Laboratory of intracellular calcium signaling National Centre for Biological Sciences (NCBS), Bangalore

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

14 Jun 2019

Abstract

:

Inositol-1,4,5 trisphosphate (IP₃) is a key cellular signaling molecule that functions downstream of certain G-protein coupled receptors and links GPCR activation to changes in intracellular Ca² +. The primary cellular target of IP₃ is the endoplasmic reticulum-localized ligand-gated calcium channel, the IP₃ receptor (IP₃R). IP₃-mediated Ca²+ release from the store stimulates upon store-operated calcium entry or SOCE that occurs primarily through the newly discovered molecules STIM and Orai. My group’s interest is to understand the developmental and physiological consequences of IP₃ signaling and SOCE in neurons in the context of the whole organism. This requires that we perturb IP₃R function and SOCE specifically in neurons and not in other cell types. The ubiquitous expression of the IP₃R, as well as STIM and Orai in multiple cell types in all multicellular organisms, is a challenge for achieving this aim. Traditionally, cellular functions of ubiquitous proteins have been addressed using pharmacological methods on cells in culture. However, this approach does not allow an understanding of the physiological and/or developmental function of the targeted protein in the context of the whole organism. Sophisticated genetic tools, either available or developed by us in the fruit fly Drosophila melanogaster, have helped in understanding the consequences of cell and tissue-specific abrogation of IP₃R function as well as STIM/Orai mediated SOCE. Based on our findings of intracellular calcium signaling in Drosophila neurons we have initiated work in mammalian systems to interrogate the significance of this pathway especially in the context of certain neurodegenerative syndromes. I will discuss our recent finding this area

Speaker Bio

:

Speaker

:

Richard G M Morris,

Affiliation

:

D.Phil., CBE, FRS Yusuf Hamied Visiting Professor in India 2019

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

4 Apr 2019

Abstract

:

Many aspects of memory entail what I have called the “automatic recording of attended experience” (Morris and Frey, Phil. Trans. Roy. Soc. B, 1997). A widely-held neural model of such memory encoding (making) is that memory traces are primarily (but not exclusively) synaptic and their creation mediated by activity-dependent synaptic plasticity, as studied in the physiological phenomena of long-term potentiation (LTP) and long-term depression (LTD). Synaptic potentiation mediated by NMDA receptor triggered changes in AMPA receptor trafficking and expression has a number of features that make it an attractive storage mechanism, but the initial encoding of ‘memory traces’ at numerous synapses within in a distributed associative memory system is no guarantee that they will last, indeed it is desirable that many should not. Separate mechanisms of consolidation mediate selective memory retention – in hippocampus and other brain areas (keeping). These ideas date back to Hebb’s (1949) concept of “cell-assemblies” and are supported by substantial contemporary work.

In this presentation, I shall touch on three new studies from my group concerning (1) silent learning; (2) differential patterns of social learning during dominance encounters between FRMP knockout and wild-type rats in an animal model of Fragile-X; and (3) new behavioural studies of synaptic tagging and capture (STC; Frey and Morris, Nature 1997) from the perspective of the modulation of memory retention by catecholamines. In different ways, these studies (1) challenge aspects of the Hebbian framework (Rossato et al, Current Biology, 2018), (2) encourage us not to adopt too deterministic a view of even single-gene abnormalities (Saxena et al, Proc. Roy. Soc. B, 2018), and (3) raise questions about the original of novelty-associated catecholaminergic modulating signal in hippocampus (Takeuchi et al, Nature, 2016).

Prof. Richard G M Morris is supported by a European Research Council Advanced Investigator Grant and a Wellcome Trust Advanced Investigator Award.

Speaker Bio

:

Speaker

:

Dr. Sufyan Ashhad

Affiliation

:

University of California, Los Angeles

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

26 Mar 2019

Abstract

:

While now well established that the preBötzinger Complex (preBötC) is the kernel of breathing rhythmogenesis in mammals, the underlying mechanisms remain a mystery. Two iconic hypotheses for preBötC rhythmogenesis, i.e., that the rhythm is generated by pacemaker neurons or by simple circuits dependent on inhibition, including post-inhibitory rebound, are not supported by experimental tests. In this talk, experimental evidence will be presented for an alternative (though non-exclusive) hypothesis, that the rhythm is an emergent property of the preBötC microcircuit. Specifically, we assessed preBötC network dynamics by recording synaptic inputs to preBötC neurons under respiratory rhythmic and non-rhythmic conditions in vitro slices from the neonatal mouse. Our analysis uncovers a dynamic reorganization of preBötC network activity correlated with and, we hypothesize, essential to, rhythmicity. In each cycle under normal conditions, an inspiratory burst (I-burst) emerges as a result of a transition of (presumptive) rhythmogenic preBötC neurons from aperiodic uncorrelated population activity to periodic synchronization during pre-inspiration; the process repeats, resulting in a rhythm. Strikingly, in a non-rhythmic slice, antagonizing GABAA receptors reinitiates this periodic synchronization and consequent rhythm, while simultaneously inducing a higher conductance state in the downstream preBötC output neurons. This co-emergence of input synchrony and higher conductance state in the output neurons unveils a novel network mechanism for generation of a propagating rhythmic breathing pattern. We posit that this evolving synchronization of preBötC activity, in each cycle, can play a critical role in binding of breathing rhythm with other brain functions through respiratory corollary discharge.

Speaker Bio

:

Speaker

:

Dr. Saurabh Bose

Affiliation

:

University of Canterbury, New Zealand

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

8 Mar 2019

Abstract

:

Inorganic emulation of organic biological brain holds immense promise to revolutionize the way modern computers process information and perform computations. Based upon spiking neuronal models of brain, reconfiguration and restructuring of conventional complementary-metal-oxide-semiconductor (CMOS) transistor chips has led to initial success. Alternatively non-CMOS approach, primarily based on memristors in cross-bar geometries, have resulted in successful supervised and un-supervised learning paradigms. Unfortunately, the functionality, adaptability and scaling of brain relies heavily upon local learning rules, implementation of which in cross-bar and CMOS structures is hindered by rigid fan-out factors. In contrast, complex networks with hierarchically adaptable connectivity between network elements have been proposed to implement such local learning scheme.

In this talk I will discuss our approach of utilizing the percolating networks of nanoparticles, poised at the edge of a phase transition, which naturally incorporate the complexity essential for brain like functionality. Variation of the strength and duration of the electric field stimulus applied to this network of synapse-like atomic-switches allows us to tune the switching dynamics. I will discuss our recent results on mechanism behind the individual switching elements, fundamental understanding of which is essential for any practical implementation. The emergent switching dynamics can be utilized for neuromorphic learning and pattern recognition in the reservoir computing paradigm.

Speaker Bio

:

Speaker

:

Debanjan Dasgupta

Affiliation

:

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

04:00 PM

Date

:

7 Mar 2019

Abstract

:

Intensity fluctuations inherent to natural odour plumes are strongly modulated by the turbulent airflows in which they are carried. Odour plumes therefore hold rich temporal dynamics of odour concentration variations, which contain information about the location and nature of an odour source. It has, therefore, been hypothesised that animals could process the temporal dynamics of natural odour plumes in order to navigate and perform odour scene segmentation.

We used dual-energy photoionisation recording to understand the temporal features of odour plumes that are of potential behavioural salience during odour scene segmentation. We observe that temporal correlation of odour plume concentrations can be used to distinctly separate between plumes arriving from a single source to that arriving from different sources separated by some distance in outdoor as well as in similar conditions indoors. To test whether mice are capable of using these temporal correlations to determine odour source separation, we developed a high-bandwidth multichannel odour delivery device capable of replicating many of the temporal features found in odour plumes. In conjunction with a high-throughput behavioural conditioning system (AutonoMouse) we trained mice (n=36) to discriminate between pairs of odours with a range of temporal correlations. Trained mice were reliably capable of discriminating correlation structure at frequencies well over the sniff rate (>15 Hz).

The high-throughput nature of these behavioural experiments allowed us to determine the psychophysical limit of perception for temporal correlation between odours, and therefore to define an appropriate stimulus range to investigate olfactory bulb representation of these stimuli. In vivo whole-cell patch-clamp recordings from mitral/tufted cells showed segregated responses depending on the correlation of odour stimuli. Further, we observed that differently sniff-coupled neurons depicted a distinct physiological difference in their reaction to the correlation structure of the stimuli.

We conclude that information of temporal correlations between odours is present in the output neurons of the olfactory bulb at sub-sniff resolution. Mice are capable of utilising this information in behaviour, suggesting that perception of temporal features of odour stimuli may be a mechanism by which animals perform odour scene segmentation. Thus, olfaction is a high bandwidth sense with temporal structure containing information about olfactory space that is indeed accessible to mice.

Speaker Bio

:

Speaker

:

Dr. Vivek Tiwari

Affiliation

:

UT Southwestern Medical Center

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

11:30 AM

Date

:

13 Feb 2019

Abstract

:

MR spectroscopy (MRS) provides a unique method for non-invasive imaging of cellular and metabolic activity in living systems. Many prior conventional MRS methods that focused on easy-to-detect neurometabolites, such as choline, lactate, NAA, etc. failed in identification of ‘metabolic-reprogramming’ signatures specific to brain-tumors. Therefore, not much success was observed for clinical advancements. My current research studies focus on identifying subtle rearrangements in clinically-relevant hard-to-detect neurochemicals, such as Glycine, 2-Hydroxyglutarate (2HG), GABA and glutamate, in brain tumors and neuropsychiatric-disorders using ‘metabolite-tailored’ MRS. Beyond the simple detection, clinical utility of these biomarkers was examined in glioma patients. Glycine was found to be elevated in tumors that had contrast enhancement: a characteristic of ‘malignant’ tumors. Presence of 2HG in the tumors serves as a first imaging ‘oncogenic biomarker’, bypassing the need of a biopsy. GABA was measured to be heterogeneously distributed in the human brain, independent of gray-matter content unlike Glycine. I will also share my idea for future research where I aim to translate novel functional-MRS (battery of MRS and functional-MRI) approaches for improved treatment outcomes in glioblastomas and evaluation of glutamate-GABA-glutamine neurotransmitter-cycling axis.

Speaker Bio

:

I am native of a town Jaunpur near Varanasi in Uttar Pradesh. I completed my bachelor’s degree (Zoology Hons.) from Banaras Hindu University (2003-2006), Masters in Biochemistry from University of Hyderabad (2006-2008). I completed my Ph.D. with Dr. Anant B Patel at CCMB Hyderabad (2008-2014) where I worked on understanding cerebral metabolism in Alzheimer’s mouse brain using NMR spectroscopy. I moved to UT Southwestern Medical Center, Dallas, Texas USA in Prof. Choi’s group in 2014 December as a postdoc fellow. Received the prestigious ‘Magna cum Laude’ and ‘Suma cum Laude’ merit awards at International Society for Magnetic resonance in Medicine consecutively in the year 2016 and 2017

Speaker

:

Dr. Sharika KM

Affiliation

:

University of Pennsylvania

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

7 Feb 2019

Abstract

:

According to the social brain hypothesis, primate brains evolved in size to adapt to the increasing demands of navigating a complex social network. Recent evidence has also shown how both social stress and loneliness can have measurable consequences to an organism’s fitness. However, the biological basis of how social contexts influence our day-to-day decision-making as well as impact health and life outcomes is still unclear. Using a combination of naturalistic laboratory tasks and physiological tools in human and non-human primates, I examined how an affective and cognitive understanding of another individual can play into the decisions we make for self and other. Specifically, I recorded the activity of neurons in the anterior cingulate cortex (ACC) – an area associated with the affective component of pain in humans – while rhesus macaques performed a novel social decision-making task. Neuronal activity in the ACC gyrus was found to be sensitive to not only the valence of outcomes for self but also those observed for a conspecific. Further, an oral dose of acetaminophen (a key ingredient in common painkillers like paracetamol) reduced this sensitivity for both self and other, consistent with the idea of 1) analgesics interfering with the normal processing of affect associated with self and other outcomes and 2) shared mechanisms evaluating the valence of outcomes for self and other. In a separate study, to understand whether activation of shared physiological responses in multiple individuals affect group outcome, I recorded physiological data (including heart rate, respiration and skin conductance response) from groups of people performing a collective decision-making task. Preliminary results suggest that groups that arrived at a correct consensus answer had greater heart rate synchrony when compared to those that did not, highlighting the role of shared physiological correlates in regulating group outcomes. In sum, my research examining the neural underpinnings of social decision-making aims to help expand our understanding of optimal social behavior for improved health and life outcomes.

Speaker Bio

:

Sharika KM did her Bachelors in Biochemistry from University of Delhi and Master’s in neuroscience at the National Brain Research Center (NBRC), Gurgaon. She stayed on to pursue her PhD. in NBRC where she used psychophysics and Transcranial Magnetic Stimulation to study how the brain plans sequential eye movements. She is currently a post-doc in the Neuroscience department of the Perelman School of Medicine, University of Pennsylvania, USA and is excited to present her recent work on understanding the neural mechanisms of social decision-making in humans and non-human primates.

Speaker

:

Dr. Arjun Ramakrishnan

Affiliation

:

Research Associate in the Department of Neuroscience at the University of Pennsylvania

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

5 Feb 2019

Abstract

:

Sensitivity to reward is a fundamental mechanism that allows living organisms to navigate an ever-changing environment. Severe changes in reward sensitivity and as a result, the decisions and actions one makes, has been associated with many mental health conditions like depression and bipolar disorder. To understand how rewards influence actions, I recorded from neurons that are involved in generating actions in nonhuman primates. These experiments revealed that neurons involved in action planning co-represented reward, demonstrating an intricate interplay between reward sensation and action planning. To understand how reward-related information is factored in to the decision process, a paradigm in which participants gambled for monetary gains and losses was developed. Behavior in the task revealed robust individual differences in reward sensitivity. A computational framework was developed to model the decision process and to extract parameters indicative of the participants’ biases in decision making. These results may aid in the determination of biomarkers to monitor subtle changes in reward-based decision making that could enable early diagnosis of mental health conditions like depression and anxiety.

Speaker Bio

:

Arjun is a Research Associate in the Department of Neuroscience at the University of Pennsylvania. Arjun holds a Bachelor of Engineering in Telecommunications from BMS College of Engineering, India; Ph.D. in Neuroscience from National Brain Research Centre, India; and gained postdoctoral experience in Neuro-engineering from Duke University. As an engineer by training and a passionate neuroscientist by practice, he enjoys developing novel technology at the interface of these two fields. By studying the neural mechanisms underlying everyday decisions we all make, he aims to determine inexpensive yet reliable biomarkers to diagnose and monitor highly prevalent and debilitating mental health conditions like depression and anxiety. As a scientific advisor, he is closely associated with a startup company based in Philadelphia – Neuroflow LLC — that aims to develop digital health solutions by leveraging biometric data to provide insights into the user’s physiological and mental states. He is the co-founder of Cogwear, LLC, a UPenn-based startup that is developing a mobile, wearable EEG device with dry, nanowire sensors, that will enable high-quality continuous monitoring of brain states. Previously, by teaming up with Miguel Nicolelis, a pioneer in brain-machine interfaces, he was instrumental in demonstrating the first Brainet – a shared brain-machine interface to jointly achieve a common goal.

Speaker

:

Prof. Michael Hasselmo

Affiliation

:

Boston unviversity

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

18 Jan 2019

Abstract

:

Episodic memory is defined as memory for events occurring at a specific time and place. Neurophysiological recordings in behaving rodents from brain regions involved in episodic memory demonstrate neuronal response properties that may code spatial location and elapsed time. This includes the coding in entorhinal cortex and hippocampus of spatial location by place cells (O’Keefe and Burgess, 1996) and grid cells (Hafting et al., 2005; Stensola et al., 2012). Many of these cells also code the temporal intervals during behavioral tasks (Kraus et al., 2013; 2015). Models of the coding of spatial location utilize either integration of running speed and direction or the sensory computation of angle and distance of visual features on environmental boundaries. These models draw on data about the neurons that respond to head direction (Taube et al., 1990), neurons that respond to running speed (Kropff et al., 2015; Hinman et al., 2016) and neurons that respond to environmental boundaries in allocentric coordinates (Solstad et al., 2008; Lever et al., 2009) or that respond to boundaries in egocentric coordinates (Hinman et al., 2017). Experimental data shows that alterations of subcortical input can impair the responses of neurons coding space (Brandon et al., 2011; Winter et al., 2015) and time (Wang et al., 2014). Experimental data and computational modeling have explored potential cortical and subcortical mechanisms for the neural coding of time and space, addressing how network dynamics could contribute to memory of location and time (Burgess et al., 2007; Burak and Fiete, 2009; Hasselmo, 2009; Howard et al., 2014), or how grid cells and boundary cells alter their coding in response to sensory input about environmental features (Raudies and Hasselmo, 2015; Campbell et al., 2018).

Speaker Bio

:

Speaker

:

Dr. Abhilasha Joshi

Affiliation

:

University of California, San Francisco

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

8 Jan 2019

Abstract

:

Rhythmic neuronal activity and its precise timing across distinct brain regions is crucial for memory-guided behavior. In the hippocampal area CA1, spiking of pyramidal cells and interneurons is organized within theta (~8Hz) and gamma (~30-100Hz) frequency oscillatory timescales. I explored the theta coordinating system in mice navigating in virtual reality using a combination of extracellular multi-unit recordings and targeted single neuron juxtacellular labelling to reveal the rules of septo-hippocampal connectivity. Medial septal Teevra cells show the highest rhythmicity, are GABAergic, fire short bursts of action potentials preferentially at the trough of individual theta oscillatory cycles and preferentially target CA3 axo-axonic cells. In contrast, GABAergic Komal cells fire long bursts at the peak of theta oscillatory cycles and innervate extrahippocampal cortical areas. I propose that the cortical-region-specific GABAergic innervation by molecularly and physiologically distinct septal neuronal types is a general mechanism for the coordination of network activity, both during locomotion and immobility, enabling goal-directed behavior.

Speaker Bio

:

Speaker

:

Divya Subramaniam

Affiliation

:

PhD student, Duke University

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

4 Jan 2019

Abstract

:

The estimation of many sensory quantities is Bayesian, in that priors and likelihoods are reliability-weighted. Sensory estimates must often be mapped onto categorical decisions, however, to guide action. For instance, when crossing a street, we categorize approaching vehicles as either “too close” or “safely far away,” informing our decision to stay on the curb or step into the road. A simple model of static, binary decision-making would involve mapping sensory estimates onto probabilities which are then compared to a threshold for a decision. Across every saccade, the visual system evaluates whether retinal displacement is due to the eye movement or external object movement. This judgment may be modeled as a binary decision – did the object move or not? – derived by thresholding the probability that an object moved, which is calculated from an estimate of retinal displacement and object movement priors. We previously showed that priors about the probability of object movement are exploited for this purpose (Rao et al. 2016). Here, we test the hypothesis that they are combined with sensory-driven likelihoods in a Bayesian manner.

Human subjects fixated a central cross, made a saccade to a peripheral target, and reported whether it had moved during the saccade. The probability of target movement was indicated by the fixation cross color. In Experiment 1, subjects were first trained on priors (0.1 or 0.9) with feedback in blocks of trials. Then, prior use was probed with low- and high-noise targets in a block with the same fixation colors but 0.5 veridical probability of movement. Consistent with a Bayesian framework, subjects used their learned priors in the high-noise but not the low-noise condition. The same result would be found, however, if priors were being unlearned with stronger expression of extinction on low-noise trials. Experiment 2 tested this possibility with low- and high-noise probe trials interspersed in longer training blocks to maintain the priors. Surprisingly, priors were used more in the low-noise than in the high-noise condition, suggesting that reliability-weighting does not extend to probability estimates for binary decisions. Instead, a learning-based model replicates the results. In Experiment 3, subjects used a mouse cursor to report the target’s postsaccadic location (no binary decision required). As expected, priors influenced location estimates more for noisier targets. Taken together, our results suggest that when judging the stability of objects across saccades, the motif of reliability-weighting at the sensory level is lost in the mapping to probabilities used for decisions.

Speaker Bio

:

Speaker

:

Dr. Megha Sharda

Affiliation

:

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

3 Jan 2019

Abstract

:

Human brain development is a complex and dynamic process. Advances in brain imaging are increasingly being used to study how maturational processes interact with experience and lead to sophisticated cognitive outcomes such as language and music. However, the heterogeneity underlying the emergence of these functions often leads to significant challenges in the translation of findings into concrete improvements in well-being. Music is a powerful multimodal tool that can provide useful insights into both brain development and neuroplasticity. On one hand, music shares behavioural and neural overlap with ubiquitous functions such as speech and sensorimotor integration, allowing investigation of these processes in populations where an impairment might be observed. On the other hand, its universal nature provides a novel paradigm to study individual differences in learning and plasticity in global populations. In the current talk, I will highlight behavioural, neuroimaging and clinical findings exploiting the overlap between speech, sensorimotor learning and music in individuals with autism that have led to the development of an intervention to improve communication. I will also share some recent work on brain connectivity in musical prodigies who acquire exceptional expertise in a short period of time. Prodigies provide a unique cross-sectional paradigm for investigating the interaction of pre-existing and acquired factors in the emergence of sensorimotor expertise, free of the relative confounds of practice and development. The link between sensorimotor learning and musical expertise can thus be studied to investigate individual differences in skill acquisition and help in identification of optimal time-points for early music education. Thus, capitalizing on the heterogeneity of a variety of neurodevelopmental populations using such interdisciplinary approaches can identify critical milestones where relevant educational and therapeutic interventions may be employed for the greatest benefits.

Speaker Bio

:

Speaker

:

Prof. Gautam Awatramani

Affiliation

:

Univ of Victoria, Canada

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

13 Dec 2018

Abstract

:

Understanding how neural circuits in the brain compute information not only requires determining how individual inhibitory and excitatory elements of circuits are wired together, but also a detailed knowledge of their functional interactions. Recent advances in optogenetic techniques and mouse genetics now offer ways to specifically probe the functional properties of neural circuits with unprecedented specificity. Perhaps one of the most heavily interrogated circuits in the mouse brain is one in the retina that is involved in coding direction (reviewed by Mauss et al., 2017; Vaney et al., 2012). In this circuit, direction is encoded by specialized direction-selective (DS) ganglion cells (DSGCs), which respond robustly to objects moving in a ‘preferred’ direction but not in the opposite or ‘null’ direction (Barlow and Levick, 1965), which we now know relies on the coordination of three transmitter systems: glutamate, GABA and acetylcholine (ACh). In this talk, I will present an in-depth functional characterization of the direction selective circuit in the mouse retina. I will discuss how the ‘coarse’ and ‘fine’ spatiotemporal coordination of inhibition and excitation shapes directional selectivity.

Barlow, H.B., and Levick, W.R. (1965). The mechanism of directionally selective units in rabbit’s retina. J Physiol 178, 477-504.

Mauss, A.S., Vlasits, A., Borst, A., and Feller, M. (2017). Visual Circuits for Direction Selectivity. Annu Rev Neurosci 40, 211-230.

Vaney, D.I., Sivyer, B., and Taylor, W.R. (2012). Direction selectivity in the retina: symmetry and asymmetry in structure and function. Nat Rev Neurosci 13, 194-208.

Speaker Bio

:

Speaker

:

Dr. Sangeeta Nath

Affiliation

:

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

6 Dec 2018

Abstract

:

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases. Our research works showed that progressive pathology development in AD is due to direct neuron-toneuron transmission of amyloid-β oligomers. Gradual accumulations of non-degradable oligomers in lysosomes enhance its progression. We have also observed the formation of TNTs during neuron-toneuron transfer. Interestingly, toxic oligomers accumulated stressed cells appear to form TNT like protrusions towards healthy cells. From several reports, it is now well established that neurodegenerative proteins follow common trends similar to prions like self-propagation and cell-tocell transmission. Even transfer of neurodegenerative aggregates via TNTs such as PrPSc, α-synuclein, tau and polyQ have recently been reported. However, molecular basis of TNTs formation in response to lysosomal accumulation of amyloid aggregates is unexplored. Efforts are now on understanding how lysosomal membrane leakage, due to accumulation of toxic aggregates, might induce formation of TNTs.

Speaker Bio

:

Speaker

:

Kavita Babu

Affiliation

:

Institute of Science Education and Research (IISER), Mohali, India

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

10.00 AM

Date

:

20 Nov 2018

Abstract

:

Normal synaptic transmission is required for the regular functioning of an organism. Presynaptic neurotransmitter release and postsynaptic receptor maintenance are both important for optimal synaptic transmission to take place. At the C. elegans neuromuscular junction (NMJ), excitatory neurotransmission occurs through the acetylcholine neurotransmitter and it’s two classes of receptors; the homomeric nicotinic acetylcholine receptors (AChR/ACR-16) and the levamisole sensitive heteropentameric receptor subunits (LAChRs) (reviewed in (Rand, 2007)). We are interested in understanding the molecules and mechanisms required for maintaining normal levels of these postsynaptic receptors at the NMJ. Claudins are a class of transmembrane tetraspan proteins that function as components of the tight junction in epithelial cells. I will discuss our recent findings on two claudin-like genes in C. elegans and their role in maintaining normal levels of acetylcholine receptors at the NMJ. My talk will go on to elaborate on the mechanism of how these claudins functions at the NMJ. Briefly, one of the identified claudin-like gene, hpo-30, is required to maintain normal LAChR levels at the NMJ and appears to function through the cell surface molecule Neuroligin to maintain receptor levels (Sharma et al., 2018). The second claudin-like protein, HIC-1, functions by regulating Wnt secretion from motor neurons, which in turn affects the delivery of AChR/ACR-16 at the NMJ (Babu et al., 2011; Jensen et al., 2012; Pandey et al., 2017; Tikiyani, 2018). My talk will elaborate on the identification of a binding partner for HIC1, Neurabin/NAB-1, and how HIC-1 and NAB-1 function together to maintain Wnt secretion and hence AChR/ACR-16 levels at the C. elegans NMJ (Tikiyani, 2018). Overall, our data suggests that in addition to their role at the tight junctions of epithelial cells, claudins play a very important role at the synapse to allow for maintaining normal postsynaptic receptor levels and hence normal functioning of neuromuscular synapses.

References

Babu, K., Hu, Z., Chien, S.C., Garriga, G., and Kaplan, J.M. (2011). The immunoglobulin super family protein RIG-3 prevents synaptic potentiation and regulates Wnt signaling. Neuron 71, 103-116. Jensen, M., Hoerndli, F.J., Brockie, P.J., Wang, R., Johnson, E., Maxfield, D., Francis, M.M., Madsen, D.M., and Maricq, A.V. (2012). Wnt signaling regulates acetylcholine receptor translocation and synaptic plasticity in the adult nervous system. Cell 149, 173-187. Pandey, P., Bhardwaj, A., and Babu, K. (2017). Regulation of WNT Signaling at the Neuromuscular Junction by the Immunoglobulin Superfamily Protein RIG-3 in Caenorhabditis elegans. Genetics 206, 1521-1534. Rand, J.B. (2007). Acetylcholine. WormBook, 1-21. Sharma, P., Li, L., Liu, H., Tikiyani, V., Hu, Z., and Babu, K. (2018). The Claudin-like Protein HPO-30 Is Required to Maintain LAChRs at the C. elegans Neuromuscular Junction. The Journal of neuroscience : the official journal of the Society for Neuroscience 38, 7072-7087. Tikiyani, V., Lei, L., Sharma, P., Liu, H., Hu, Z., and Babu, K. (2018). Wnt secretion is regulated by the tetraspan protein HIC-1 through its interaction with Neurabin/NAB-1. Under Revision.

Speaker Bio

:

Speaker

:

Dr. Ishaan Gupta

Affiliation

:

Neuroscience Weill Cornell Medical College, New York

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

26 Oct 2018

Abstract

:

A Human body has approximately 37.2 trillion cells, each having exactly the same DNA sequence or the set of instructions to make up the entire body. The cells in our legs and the cells in our eyes have exactly the same DNA, yet perform very different functions.

How does the same DNA give rise to very different cell types?
What happens during the development of a complex organ like the brain?
What happens to different cell types of the brain in diseases such as dementia?

I will try to give some insights into these above questions using the novel methods that I have been working on during my research career.
In particular, I will focus on new single-cell and single-molecule RNA sequencing technologies that enable us to visualize the complete results of a gene’s expression (transcriptional/translational output) from thousands of single cells in the complex tissue such as the mammalian brain.

I am going to end with new design principles of gene expression; discovered through these methods; which may explain how specific functional modules emerge to give different cell types in health and disease.

Speaker Bio

:

Speaker

:

Prof. Stuart Baker

Affiliation

:

Newcastle University

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

12:00 PM

Date

:

26 Oct 2018

Abstract

:

Speaker Bio

:

Speaker

:

Dr. Rajnish P Rao Bernstein

Affiliation

:

Center for Computational Neuroscience, Humboldt University of Berlin

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

9 Oct 2018

Abstract

:

Complex social interactions are observed in gregarious species during the display of dominance hierarchies, mating and parental behaviors. The ability to recognize and distinguish between different individuals (e.g. a potential mating partner or a competitor for resources/mates) in these contexts is vital. The neuronal basis of social recognition therefore has been the subject of extensive investigation. In their seminal study on the patient HM, Scoville and Milner suggested that the Hippocratic formation was involved in the processing of social memories. Indeed, individual selective cells were reported in the now famous “Jennifer Aniston cell” report by Quiroga et al. However, lesion evidence on the involvement of the rodent hippo campus in social memory has been contradictory. In addition, several studies failed to find any indication of social responses in the dorsal hippo campus. In this study, we investigated the role of the ventral hippo campus. In an ethological approach, we used interacting rats to acquire a rich data set with high spatio-temporal resolution. In a population of ventral CA1 neurons, we observed large modulations by con specific (but not object) presence. They were repeatable when the same con specific was presented and differential when different con specifics were presented. These were not related to behavioral, attentional or spatial contingencies. The vCA1 neurons showed modulation to multi sensory inputs and this potentially contributes to their ability to discriminate between the sex and individual presented. Con specific presence on the other hand, had little or no effect on dorsal CA1 activity. We think these findings are of importance for understanding the neuronal substrate of social recognition. The results deepen our understanding of the regional specialization of the hippo campus and suggest that social responses map onto the poorly explored ventral pole of the rodent hippo campus. Further, they add to the growing evidence that hippocampal activity cannot be reduced to purely spatial activity patterns.

Speaker Bio

:

Speaker

:

Dr. Samit Chakravarthy

Affiliation

:

University of Leeds

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

20 Sep 2018

Abstract

:

In my group, we have been exploring the rules of plasticity amongst the pathways that govern motor activity, via the spinal circuits, related to the hands and legs. Our focus is on the modulation of these spinal circuits during a task and when in disease or dysfunctional states like spinal cord injury, cerebral palsy or strokes. We take a mechanical view of the nervous system, exploring the interaction between muscles, neuronal pathways and the environment in both animals and humans, examined by studying the functional outputs from these. We have established the role of co-operation and competition between pathways in short and long temporal scales for effective recovery from injuries influencing motor output, especially during cerebral palsy.

In this talk, I will provide some basic evidence for the ideas above and how we are currently developing tools to identify the pathways active in people during specific tasks – synergies, but observing changes that occur within a period enough for a single synaptic event to influence the output without the involvement of the brain. I will give you some evidence for the change in inputs to the same muscles during different but almost identical tasks, suggesting tools that could be useful to allow both clinicians and engineers to develop calibration measures for individual patient. In other words, help stratify the population and diagnosis to know their current state of plasticity, allowing better therapeutics.

The wishful thinking here is that it is likely to also aid in defining tools that are more effective in carrying out faster recovery from perturbation or adjusting to the demand.

Speaker Bio

:

Speaker

:

Krithika Mohan

Affiliation

:

PhD Candidate, University of Chicago

Venue

:

CNS Ground Floor Seminar Hall

Time

:

11:30 AM

Date

:

21 Aug 2018

Abstract

:

Primates exhibit exceptional flexibility in their behavior. Indeed, we can use the same visual input to guide a variety of decisions and actions. Yet, these flexible behaviors are supported by neuronal computations that are not understood. To understand the neural basis of flexibility, we investigate the posterior parietal cortex – an area of the macaque brain involved in spatial attention, decision making and visual categorization. In a categorization task-switching paradigm, we recorded from the posterior parietal cortex (area LIP) of non-human primates trained to alternate between motion categorization tasks in which they categorized the same random-dot motion stimuli under two different schemes – with a hand movement versus an eye-movement depending on an active, cued rule. Single neuron responses were heterogeneous, non-linear and exhibited mixed tuning and dynamics to various task-relevant variables. While single neurons represented complex mixtures of task-relevant variables in both tasks, the neural population showed robust category selectivity that was remarkably similar across the two tasks. While category-dependent responses were conserved in both tasks, other task-relevant variables such as motion direction and choice were influenced by cognitive demands unique to the tasks at hand. Finally, recurrent neural networks trained to perform task-switching between categorization tasks revealed that dynamical landscapes converged during the “shared” decision epoch and diverged during the “independent” choice epoch. Our findings demonstrate that parietal neural circuits can mediate flexible task-switching by differentially formatting relevant information in a task-dependent manner.

Speaker Bio

:

Speaker

:

Dr. Shovamayee Maharana

Affiliation

:

Max Planck Institute of Molecular Cell Biology and Genetics, Dresden

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

24 Jul 2018

Abstract

:

Phase separation of prion-like RNA binding proteins (RBPs) into liquid droplets has been proposed to underlie the formation of membrane-less compartments, such as stress granules and processing (P) bodies in the cytoplasm or paraspeckles and Cajal bodies in the nucleus. The defining feature of prion-like RBPs are low complexity sequences, which drive liquid droplet formation through multivalent self-interactions. When these proteins localize in the nucleus, they are highly soluble and form physiological membrane-less compartments. However, when mislocalized to cytoplasm, they form solid-like aggregates that cause age-related neurodegenerative diseases. This raises two important questions: what keeps these proteins soluble in the nucleus and what prevents the conversion of liquid nuclear compartments into pathological aggregates? Here, I used in vitro reconstitution approaches along with live cell imaging to characterize the phase behavior of the prion-like proteins FUS, TAF15, EWSR1, hnRNPA1 and TDP43. I find that the ability of these RBPs to phase separate is strongly dependent on the RNA/protein ratio. We show that the high RNA concentration in the nucleus keeps prion-like RBPs in a soluble state, whereas the low RNA concentration in the cytoplasm promotes phase separation. I further demonstrate that RNA prevents the conversion of RBPs from a liquid to a solid-like aggregated state. Based on these findings, I propose that RNA regulates the phase behavior of prion-like RBPs and controls the material properties of liquid droplets. This suggests that changes in RNA homeostasis or alterations in RNA-binding abilities due to disease mutation could lead to severe protein aggregation diseases. References: Maharana, S., Wang, J.*, Papadopoulos, D.K.*, Richter, D., …, Tomancak, P., Hyman, A.A., Alberti, S. RNA buffers the phase separation behavior of prion-like RNA binding proteins. Science (2018). *Equal Contributors. 2) *Patel, A., *Lee, H.O., Jawerth, L., Maharana, S.,…, Hyman, A.A., Alberti, S. A liquid-to-solid phase transition of the ALS protein FUS accelerated by disease mutation. Cell, 5 :1066-1077 (2015) *Equal Contributors.

Speaker Bio

:

Speaker

:

Dr.Dhrubjyoti Chowdhury

Affiliation

:

Johannes Hell Lab, University of California Davis

Venue

:

Seminar Hall, Ground Floor, Centre for Neuroscience

Time

:

4:00 PM

Date

:

19 Jul 2018

Abstract

:

Ionotropic glutamate receptors (iGluRs) form the core of excitatory synaptic transmission in the mammalian brain and underlie sensory processing as well as learning and memory. Comprising of the two major subtypes, AMPARs and NMDARs, the synaptic abundance of these receptors is tightly regulated by neuronal activity via trafficking and anchoring mechanisms. Protein-protein interactions and posttranslational modifications of both the receptor and its interacting partners represent key molecular mechanisms behind the dynamic tuning of synaptic iGluR content necessary to respond appropriately to extracellular cues. My research investigates such mechanisms behind activity-dependent regulation of the synaptic abundance of iGluRs. I identified an interplay between palmitoylation of postsynaptic density -95 (PSD-95), the scaffolding protein anchoring AMPARs, and its interaction with calcium/Calmodulin as a central molecular mechanism controlling synaptic localization of AMPARs in homeostatic synaptic plasticity. In addition, I dissected the molecular details regulating the endocytosis of GluN3A-containing “nonconventional” NMDARs with implications for synapse maturation. I identified an atypical endocytic motif within GluN3A carboxyl-terminal domain, its phosphorylation by the tyrosine kinase, Src, and how it regulates GluN3A surface expression in cultured neurons. Future work is directed towards understanding the molecular details of endosomal trafficking in regulating iGluR synaptic homeostasis, an emerging focus in the field of severe neurological disorders.

Speaker Bio

:

Speaker

:

Arun Narasimhan

Affiliation

:

Cold Spring Harbor Laboratory, New York NY.

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

18 Jul 2018

Abstract

:

The somato-dendritic morphology is a classic feature in defining neuronal types. While morphologies of smaller subsets of anatomical regions have been studied in more detail, we aim to study the morphology and axonal projections of the pyramidal cells of the entire mouse neocortex using a custom-built Oblique Light Sheet Tomography (OLST) a whole-brain volumetric imaging platform operating on the principle of light sheet fluorescence microscopy, that allows us to image an adult mouse brain within ~14 hrs at 0.4 x 0.4 x 2.5 μm voxel resolution with overlapping regions for image registration and reconstruction. To identify individual neurites in our images, we obtain a sparse labeling of the pyramidal cells in Emx1-Cre mice using viral injections of Cre-dependent reporter AAV viruses. We then developed deep neural networks that binarized the raw images and subsequently obtained the skeletons of neuronal arbors automatically. This framework enables us to study fine morphology and the spatial patterns of cortical neurons at a high-throughput, a prerequisite for identification of cell types.

Speaker Bio

:

Speaker

:

Dr. Debasis Das

Affiliation

:

University of Wisconsin, Madison

Venue

:

Seminar Hall, Ground Floor, Centre for Neuroscience

Time

:

4:00 PM

Date

:

12 Jul 2018

Abstract

:

A synchronized overall function of human body requires precise spatio-temporal regulation of the release of hormones, neurotransmitters, etc. To mediate the intercellular communication, these chemicals are released into the extracellular space through the ephemeral fusion pores. Little is known about the mechanisms that determine size and kinetic properties of these transient structures. The small unstable pores may allow only transient release of small hormones from neuroendocrine cells and could dictate the rate of neurotransmitter release from nerve terminals to reduce postsynaptic responses. Here I will describe a novel approach that allowed us to trap nascent recombinant fusion pores in their metastable states to monitor their micro-sec dynamics for the first time. I will thus address fundamental questions about the structure-function relation of fusion pore, which were impossible to study before. This has initiated a major revision of how chemical messengers are released and has opened up new direction to study the fusion pore properties.

Speaker Bio

:

Speaker

:

Prof. Dean Buonomano

Affiliation

:

University of California, Los Angeles

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

9 Jul 2018

Abstract

:

Much of the information the brain processes and stores is temporal in nature—a spoken word or a handwritten signature is defined as much by how it unfolds in time as by its spatial structure at any moment. The brain seamlessly assimilates and process temporal information, an ability that is critical to most behaviors: from reward anticipation to sensorimotor processing. We have proposed that timing on the scale of milliseconds to seconds relies on the intrinsic dynamics of recurrent neural networks (RNNs). Under this view information is stored and generated by dynamic attractors—locally stable neural trajectories. Starting from RNN models that are in a chaotic regime, we show that by tuning the recurrent weights of RNNs it is possible to generate stable neural trajectories that can solve both sensory and motor tasks. We provide experimental support for the hypothesis that timing is an intrinsic computation of neural networks by demonstrating that in vitro cortical networks can “learn” simple temporal patterns. Overall we propose that in contrast to the conventional view that memories are stored as static fixed-point attractors, that many computations emerge from the voyage through neural state space as opposed to the destination.

Speaker Bio

:

About Speaker : He is the author of books brain bugs and your brain is the time machine. For more about his lab please visit : http://www.buonomanolab.com/

Speaker

:

Dr. Vivek Tiwari

Affiliation

:

University of Texas Southwestern Medical Center

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

11:30 AM

Date

:

13 Jun 2018

Abstract

:

Speaker Bio

:

Speaker

:

Dr. Vivek Swarup

Affiliation

:

Program in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

25 Apr 2018

Abstract

:

Mutations causing frontotemporal dementia have been identified, but disease mechanisms are not well understood. We reasoned that defining transcriptional networks dysregulated in genetic models of disease would inform mechanistic understanding and conducted mRNA and miRNA sequencing of multiple brain regions from F1 crosses of a TauP301S mouse model on three divergent strains to reduce effects caused by genetic background. Network analysis identified two co-expression modules that were conserved across multiple model systems and in human post mortem brain from dementia patients. We show that a hub of a putative regulatory miRNA module re-capitulates mRNA co-expression patterns associated with disease state and induces neuronal cell death. We use network modules to identify a probe compound and show that it has the predicted protective effect. Collectively, we identify conserved, disease relevant co-expression networks representing convergent changes in dementia, and a hub miRNA as a novel regulator of these networks and neurodegeneration.

Speaker Bio

:

Speaker

:

Dr. Rangaprakash D

Affiliation

:

University of California, Los Angeles

Venue

:

CNS Seminar Hall, Ground Floor

Time

:

4:00 PM

Date

:

17 Apr 2018

Abstract

:

Emotions arise when the brain judges a situation as positive or negative towards achieving its goals. Circumstances often diverge from goals; hence, brain mechanisms exist for the regulation of emotion. Given that emotions are closely tied to hedonic as well as goal-directed behavior, emotion regulation is a fundamental construct of many cognitive processes. To understand its neural mechanisms at the systems-level, prior studies have identified brain regions important for emotion regulation. However, an understanding of the underlying network mechanisms, critical for developing accurate mechanistic models of regulation, have not emerged.
Functional magnetic resonance imaging (fMRI) is a non-invasive modality that can capture brain activity throughout the brain with high spatial resolution (about 2 mm3), making it one of the suitable tools to probe emotion regulation. This talk presents the discovery of brain network mechanisms underlying cognitive emotion regulation in healthy adults, and its disruption pattern in two clinical populations (N=66).

Using an fMRI emotion regulation task and brain connectivity modeling, we found the left middle frontal gyrus (MFG) to initiate regulation and exert control over subcortical/parietal regions. Dysregulation was characterized as an imbalance within the regulation network, with reduced prefrontal but elevated subcortical/parietal connectivity. MFG-to-amygdala connectivity was associated with self-reported success of regulation and neurocognitive functioning, as well as predictive of both. Importantly, while MFG-to-amygdala connection explained 29% variance in success of regulation, the entire regulation network taken together explained 63% variance, demonstrating that regulation is enabled through a distributed network originating in the MFG, and not merely confined to one or two pivotal regions/connections. Apart from advancing the understanding of emotion regulation in humans, implications of this study include treatments targeting MFG, the source of the identified network.

Speaker Bio

:

Speaker

:

Bhavana Muralidharan

Affiliation

:

Department of Neurodegenerative Disease,
UK Dementia Research Institute, UCL, London

Venue

:

CNS Seminar Room

Time

:

4:00 PM

Date

:

3 Apr 2018

Abstract

:

The cerebral cortex is the seat of sensory perception, decision-making, language, learning and memory. For a functional cerebral cortex in adulthood, a diverse number of neurons and glia are to be produced adequately during development. Chromatin level regulations play a very crucial role in the fate specification of neurons and glia. Several neurodevelopmental disorders stem from mutations or perturbations to the process of chromatin regulation.

Yet our molecular understanding of these mechanisms is very poor in the developing brain.

To elucidate such mechanisms, I looked at the downstream targets of transcription factor (TF) Lhx2, that has distinct roles in the two regions of the cerebral cortex namely neocortex and hippocampus. In my talk I will describe how this TF along with its association with chromatin modifiers, regulates its target genes to specify a particular class of cortical neurons, which project to the spinal cord and are involved in movement, in the neocortex. Whereas, in the hippocampus, Lhx2 along with 3 other TFs participates in a complex regulatory network to ensure proper numbers of neurons and glia.

Further I will discuss how studying the global genome wide occupancy profiles of TFs and chromatin remodelers will help us understand the fine tuning of gene expression and shed light into the dynamicity of brain development.

Speaker Bio

:

Speaker

:

Dr. Prakash Devaraju

Affiliation

:

Department of Developmental Neurobiology, St. Jude Children’s Research Hospital, Memphis

Venue

:

CNS seminar hall

Time

:

4:00 PM

Date

:

13 Mar 2018

Abstract

:

The broader theme of our research is to understand the neural circuit basis of cognitive function and its abnormalities. Using a combination of electrophysiological, biochemical and imaging approaches in transgenic disease models, we narrowed on two genes involved in mitochondrial function which affect different memory circuits.  Using an electrophysiological screen, we identified Mrpl40 as a culprit gene involved in working memory disorder. Deficiency of this gene leads to abnormal mitochondrial calcium extrusion and thereby affects short term plasticity in a neural circuit involved in working memory. A candidate gene approach has implicated another nuclear gene encoding a mitochondrial protein in a circuit involved in social memory.  The talk will focus on the mitochondrial, synaptic and circuit mechanisms by which deficiency of these two genes gives rise to deficits in working and social memory.

Speaker Bio

:

Speaker

:

Dr. Srikanth Padmala

Affiliation

:

University of Maryland

Venue

:

CNS Seminar Room

Time

:

4:00 PM

Date

:

1 Mar 2018

Abstract

:

Throughout our lives, our thoughts and actions are shaped by the influence of emotional and/or motivational factors. Hence, there is a clear need to understand how emotion, motivation and cognition interact in the human brain. Knowledge of brain mechanisms underlying these interactions is not only relevant to our normal lives but also has potential clinical significance in mental disorders such as addiction, anxiety, and depression. Despite this, our understanding of how these factors interact in the brain is rudimentary. Over the past decade, my work sought to fill some of these critical gaps in our knowledge base, investigating interactions between emotion, motivation and cognition in the healthy adult human brain using behavioral and functional MRI (fMRI) techniques. During this talk, I will present a portion of this work mainly focusing on recent behavioral and neuroimaging studies investigating interactions between reward motivation and negative emotional processing during perception and attention.

Speaker Bio

:

Dr. Padmala earned his Bachelor’s degree in Biomedical Engineering from Osmania University, Hyderabad in 2001 followed by a Master’s degree in Biomedical Engineering from University of Memphis, USA in 2003. Afterwards, he worked for more than a decade in Dr. Luiz Pessoa’s laboratory of Cognition and Emotion investigating brain mechanisms of emotional perception and interactions between emotion, motivation and cognition in humans using behavioral and functional MRI techniques. Recently, as a National Science Foundation (NSF) Graduate Research Fellow, Dr. Padmala received his PhD from the inter-disciplinary Neuroscience and Cognitive Science program at University of Maryland, where he currently works as an Assistant Research Scientist.

Speaker

:

Dr.Tapan Nayak

Affiliation

:

Department of Physiology and Biophysics, SUNY at Buffalo, New York, USA

Venue

:

CNS Seminar Room

Time

:

11:00 AM

Date

:

28 Feb 2018

Abstract

:

At synapses, neurotransmitter released from nerve terminals binds ligand-gated ion channel (LGICs) receptors to produce a synaptic response. How a chemical signal is transduced to electrical signal; how neurotransmitter binding activates an ‘allosteric’ receptor and what structural elements are involved in the process? Study of neurotransmitter action on LGICs is fundamental to understand normal synapse function and the etiology of nervous system disorders. I use patchclamp, protein engineering, thermodynamics and molecular simulations to understand neurotransmitter binding and ‘gating’ (global conformational change that leads to ion channel opening) in acetylcholine receptors (AChRs) at nerve-muscle synapses. My results suggest that, in AChRs, agonist ‘affinity’ is determined by a conserved core of five aromatic residues. Affinity can be engineered by modulating the outer-zone residues at the binding site. Ligand binding either precedes (conformational selection) or follows (induced-fit) a local conformational change depending on the state of the binding site (closed vs open). ‘Efficacy’ of the receptor is a function of the agonist energy (owing to affinity) and the intrinsic gating energy. Constitutive channel activity is a manifestation of the intrinsic gating energy. Mutations, including those causing diseases, and the allosteric modulators (current therapeutics) only resettle the intrinsic gating of the receptor locally. Allosteric communication from the orthosteric agonist site (50 Å away) is transmitted as a ‘conformational wave’ to the ion channel pore. The mechanism of allosteric communication will be discussed in the light of intermediates in the transition state ensemble.

Speaker Bio

:

Speaker

:

Dr. Harini Chakravarthy

Affiliation

:

Venue

:

CNS Seminar Room

Time

:

12:00 PM

Date

:

27 Feb 2018

Abstract

:

Insulin-producing pancreatic beta cells in mice can slowly regenerate from glucagon-producing alpha cells in settings like beta cell loss, but the basis of this conversion is unknown. Moreover, it remains unclear if this intra-islet cell conversion is relevant to diseases like type 1 diabetes (T1D). We show that the alpha cell regulators Aristaless-related homeobox (Arx) and DNA methyltransferase 1 (Dnmt1) maintain alpha cell identity in mice. Within 3 months of Dnmt1 and Arx loss, lineage tracing and single-cell RNA sequencing revealed extensive alpha cell conversion into progeny resembling native beta cells. Physiological studies demonstrated that converted alpha cells acquire hallmark beta cell electrophysiology and show glucose-stimulated insulin secretion. In T1D patients, subsets of glucagon-expressing cells show loss of DNMT1 and ARX and produce insulin and other beta cell factors, suggesting that DNMT1 and ARX maintain alpha cell identity in humans. Our work reveals pathways regulated by Arx and Dnmt1 that are sufficient for achieving targeted generation of beta cells from adult pancreatic alpha cells.

Speaker Bio

:

Speaker

:

Prof. Itzhak Fried

Affiliation

:

University of California, Los Angeles

Venue

:

Faculty Hall, IISc

Time

:

4:00 pm

Date

:

19 Feb 2018

Abstract

:

Speaker Bio

:

Speaker

:

Anant Jain

Affiliation

:

Dr. Catherine Woolley’s lab, Northwestern University, USA

Venue

:

CNS Seminar Hall

Time

:

4:00 PM

Date

:

16 Feb 2018

Abstract

:

Speaker Bio

:

Speaker

:

Dr.Parthasarathy Bhagavatula

Affiliation

:

Venue

:

CNS Seminar Room

Time

:

04:00 PM

Date

:

6 Feb 2018

Abstract

:

Visually guided navigation in birds enables them to orchestrate smooth landings, fly through narrow spaces, avoid obstacles and detect targets. Our understanding about bird flight is largely targeted towards long distance navigation and migration, yet we know so little about short distance migration. I explore visually guided free flight in birds over short distances using non-invasive methods like motion capture, eye tracking, GPS trackers and inertial sensors. I explored free flight in Budgerigars, Pigeons, Peach faced love birds, African grey parrots and Red tailed hawks. The seminar I present at the Indian Institute of science will largely cover my adventures in studying birds, both in the laboratory and in the field, on two different continents.

Speaker Bio

:

Speaker

:

Dr.Shrikant Bharadwaj

Affiliation

:

Venue

:

CNS Seminar Room

Time

:

04:00 PM

Date

:

31 Jan 2018

Abstract

:

We have two eyes for a reason – our ability to perceive 3D and compute distance and direction is highly enhanced with the two eyes work together as a team. Such an ability of the two eyes to work as a team is highly dependent on the similarity of inputs in the two eyes. There are instances – physiological, pathological and iatrogenic – when such a similarity in visual inputs is disrupted. Spatially, one eye may be see this world more distorted than the other eye and such differences in distortion may also progress with time. What are the consequences of such inter-ocular differences in spatial and temporal input to the two eyes? What happens when such differences become part of one’s natural viewing? What mechanism does the visual system adopt to handle such inter-ocular differences and what implications do these have when treating patients in the clinic? These questions will be discussed in my talk with evidence for some adaptive behavior by the visual system to handle such inter-ocular differences in visual input.

Speaker Bio

:

Dr. Shrikant Bharadwaj completed his undergraduate degree in Optometry from the Elite School of Optometry, Birla Institute of Technology and Science, Pilani and a PhD in Vision Science from the University of California Berkeley School of Optometry, USA. After completing his post-doctoral training in Vision Science at the Indiana University School of Optometry, USA, Dr. Bharadwaj returned to the L V Prasad Eye Institute (LVPEI) in Hyderabad a DBT Ramalingaswami Fellow in 2009. Dr. Bharadwaj has since then established the Visual Optics research laboratory at LVPEI with the overall agenda of understanding how the optics of the eye influences spatial vision and depth vision. Dr. Bharadwaj uses a combination of experimental, behavioral and computational techniques to address this research agenda. His laboratory actively publishes research work in international peer reviewed vision science journals and the research work is generously supported by extramural grants from the Department of Science and Technology and Department of Bio-Technology and from the optical industry. Dr Bharadwaj also serves on the editorial board of Nature Scientific Reports, Optometry and Vision Science and the Indian Journal of Ophthalmology.

In addition to his research work, Dr. Bharadwaj also serves as Director of the Brien Holden Institute of Optometry and Vision Sciences, L V Prasad Eye Institute and also teaches at the institute’s Bausch & Lomb School of Optometry.

Speaker

:

Dr.Chandana Kondapalli

Affiliation

:

Post doctoral research associate, Department of Neuroscience, Columbia University

Venue

:

CNS Seminar Hall

Time

:

04:00 PM

Date

:

30 Jan 2018

Abstract

:

Alzheimer’s Disease (AD) is the most common neurodegenerative disease that causes progressive decline in cognitive function. Studies have highlighted synaptotoxic effects on excitatory pyramidal neurons (PNs) caused by oligomeric Aβ42, leading to loss of dendritic spines and altered synaptic plasticity, during the early stages of AD. Role for dysfunctional mitochondria in AD has also been postulated. However, it is unclear if there is a causal relationship between oligomeric Aβ-dependent synaptotoxicity and disruption of mitochondrial homeostasis. Moreover, the molecular pathway that connects these changes is unknown. Recent results from Franck Polleux’s lab uncovered that Aβ42 oligomers over-activate the stress-response AMP-activated kinase (AMPK) and that inhibition of AMPK protects hippocampal PNs from Aβ42-mediated spine loss in the hAPP^SWE,IND transgenic AD mouse model (J20) in vivo (Mairet-Coello et al. Neuron 2013). As a follow up to this identification, my postdoctoral work has helped in identifying that AMPK over-activation by Aβ42 oligomers also triggers spatially restricted MFF-dependent mitochondrial fission and ULK2-dependent mitophagy in PNs. In parallel, we observea striking structural remodelingof mitochondria that occurs specifically in the apical tufts dendrites of CA1 PNs, a portion of the dendritic arbor where we also detect dramatic synaptic loss in J20 mice. Overall, our project elucidates the cellular and molecular mechanisms mediating the effects of Aβ42 oligomers on mitochondrial defects, synaptic maintenance and their functional impact on hippocampal circuit in AD.

Speaker Bio

:

Speaker

:

Dr.Arunesh Saras

Affiliation

:

Department of Environmental Science, Policy and Management, University of California, Berkeley, USA

Venue

:

CNS Seminar Room

Time

:

12 PM

Date

:

29 Jan 2018

Abstract

:

Despite the frequency of seizure disorders, such as epilepsy, in the human population; the genetic and physiological basis for these defects has been difficult to resolve. We use Drosophila as an animal model to study epilepsy, where seizures can be induced by either mechanical shock or high frequency stimulation (HFS). In particular, these Drosophila mutants are described as bang-sensitive (BS) mutants. Even though several genetic seizure-suppressors have been identified for BS mutants, however, the BS mutant parabss1 caused by a gain-of-function mutation of the voltage-gated Na+ channel gene is extremely seizure-sensitive with phenotypes that have proven difficult to ameliorate by anti-epileptic drug feeding or by seizure-suppressor mutation. It has been presented as a model for intractable human epilepsy. Here we show that cacophony (cacTS2), a mutation of the Drosophila presynaptic Ca++ channel α1 subunit gene, is a particularly potent seizure suppressor mutation, reverting seizure-like phenotypes for parabss1 and other BS mutants. Seizure-like phenotypes for parabss1 may be suppressed by as much as 90% in double mutant combinations with cacTS2. Thus, cacTS2 has been identified as the strongest seizure-suppressor in Drosophila, to date. Moreover, we have recently identified mushroom body (MB), a key area for learning and memory formation, as one apparent locus of optogenetic seizure initiation in Drosophila brain. We find that the α/β lobes of MB are primarily responsible for MB seizures induction. Overall, our study shows that optogenetics can be a powerful method to study seizures in the Drosophila model.

Speaker Bio

:

Speaker

:

Dr.Bhuvanesh Awasthi

Affiliation

:

University of Glasgow, United Kingdom

Venue

:

CNS Seminar Room

Time

:

04:00 PM

Date

:

23 Jan 2018

Abstract

:

A crucial issue in the cognitive neuroscience of visual perception has centred on  the extraction and processing of relevant information from the visual environment. The influence of spatial frequency information on high-level perceptual processing remains under investigation and debate. While most previous research addresses individual roles of the spatial frequency (SF) scales (using just one SF band at a time), issues regarding the integration of these scales have remained unexplored. I used visually guided reaching and transcranial Random Noise Stimulation (tRNS) to examine low and high spatial frequency filtered face perception in healthy adults. Results from the reaching trajectories as well as the neuromodulation study demonstrate a behavioral significance and the neural primacy for low spatial frequency information in perception of faces.

Speaker Bio

:

Dr Bhuvanesh Awasthi is a cognitive scientist with particular research focus on mechanistic and functional accounts of perception, emotion and decision-making in humans. He has worked in the United Kingdom, United States of America, Russia and Australia. His early training was from the University of Pune, a Consciousness Studies Masters from BITS Pilani and a PhD from Sydney, Australia. He has been invited to present his research to a variety of audience across North America, UK, Europe, Middle East, India & Australia.

Speaker

:

Dr.Thiruma Arumugam

Affiliation

:

Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117597, Singapore and School of Pharmacy, Sungkyunkwan University Suwon Republic of Korea

Venue

:

CNS Seminar Hall

Time

:

4:00 PM

Date

:

12 Jan 2018

Abstract

:

Intermittent fasting (IF) is a dietary protocol where energy restriction is induced by alternate periods of ad libitum feeding and fasting. Prophylactic intermittent fasting has been shown to extend lifespan and attenuate the progress and severity of age-related diseases such as cardiovascular, neurodegenerative and cancerous diseases in animal models. Stroke is the second leading cause of death, and lifestyle risk factors such as obesity and physical inactivity have been associated with elevated risks of stroke in humans. Recent studies have shown that prophylactic IF may mitigate tissue damage and neurological deficit following ischemic stroke. The efficacy of IF to protect brain against neurodegenerative diseases and ischemic injury involved the coordinate upregulation of multiple neuroprotective proteins including neurotrophic factors, such as BDNF and bFGF; protein chaperones, including Hsp70 and GRP78; antioxidant enzymes, such as SOD and HO-1, down regulation of pro-inflammatory cytokines (TNF, IL-1b and IL-6) and suppression of inflammasome activation at the site of injury.  In this talk, I will summarize the data supporting the mechanisms of IF in ischemic stroke, epigenetics and neural plasticity.

Speaker Bio

:

Speaker

:

Prof.Mayank Mehta

Affiliation

:

UC Los Angeles

Venue

:

CNS Seminar Hall

Time

:

10:30 AM

Date

:

12 Jan 2018

Abstract

:

Speaker Bio

:

Speaker

:

Venkatesh N. Murthy Professor & Chair of Molecular & Cellular Biology Co-Chair,

Affiliation

:

Graduate Program in Biophysics Harvard University | 16 Divinity Ave Cambridge, MA 02138

Venue

:

CNS Seminar Hall

Time

:

4 pm

Date

:

22 Dec 2017

Abstract

:

In a cluttered sensory environment, animals must segregate objects of interest from ever varying backgrounds, and categorize them for decision making. We study this problem in the olfactory system. We have shown that laboratory mice are excellent at recognizing individual odorants embedded in unpredictable and variable background odor mixtures. We have also shown that this task is computationally straightforward – linear decoders with sparse weights acting on early sensory representations are sufficient to solve the problem. In a related task, we trained mice to categorize odors into rewarded or unrewarded odors, and asked where in the olfactory brain we can find explicit neural representation of valence (reward) category. I will present the results of these experiments and discuss their implications for odor object recognition.

Speaker Bio

:

Speaker

:

Prof. Shubha Tole,

Affiliation

:

Department of Biological Sciences, Tata Institute of Fundamental Research, Mumbai, India.

Venue

:

CNS Lecture Hall

Time

:

4 PM

Date

:

7 Dec 2017

Abstract

:

  The cerebral cortex arises from a simple sheet of neuroepithelial tissue in the embryo.  How this sheet is patterned to produce distinct cortical structures in a reliable and reproducible manner is a question of both evolution and development.   We discovered that the cortical hem, a Wnt-rich signaling center that forms at the telencephalic midline, acts as a secondary organizer in the embryonic brain, and induces the hippocampus.  Embryos that were genetically manipulated to form additional ectopic hems displayed multiple ectopic hippocampi, demonstrating that the hem is the hippocampal organizer.  How the hem itself forms and how its position is limited to the telencephalic midline therefore becomes a compelling question, because the position of the hem determines the position of the hippocampus.

               We explored interactions between three regulators of early patterning, transcription factors Foxg1, Lhx2, and Pax6, and identified early mechanisms that regulate the formation and position of the cortical hem.  Furthermore, we uncovered an unexpected and necessary suppression of Wnt-responsiveness within the hem.  That is, in order for the hem to do its job of producing Wnt signals, it must necessarily not respond to them.  Finally, we discovered that hem is itself part of a multi-component “forebrain hem system” that may have arisen as part of an evolutionary mechanism to regulate the formation of the cerebral cortex.

Speaker Bio

:

Speaker

:

Aditi Bhattacharya, PhD

Affiliation

:

Center for Brain Development and Repair Institute for Stem Cell Biology and Regenerative Medicine, UAS-GKVK campus, Bangalore

Venue

:

CNS Seminar Hall

Time

:

12PM

Date

:

5 Dec 2017

Abstract

:

Studying mRNA translation and protein expression in response to specific stimuli has been a high interest area in neurobiology for numerous years. This arises from the fact that almost every process of learning and memory, manifesting in behavioral changes, requires alterations in translational profiles and protein expression in specific cells, circuits and areas of the brain. Conversely, almost every neurological condition usually has the expression of some protein awry that contributes to it’s underlying molecular cause, either directly or indirectly. Surprisingly molecular neurobiology has garnered most of its translation information from traditional ‘whole homogenate’ studies or dissociated culture systems. I will begin with showcasing my previous work, of modulating p70 ribosomal S6Kinase 1, a key signaling integrator to translation control, helped ameliorate disease-associated phenotypes in Fragile X Syndrome, a leading cause of inherited autism and intellectual disability and using that platform to devise usable molecular biomarkers for Fragile X syndrome. I will then highlight my recent efforts at developing a method to track proteomic changes in neurons and glial from intact brain slices simultaneously using non-canonical amino acid tagging (NCAT). Two vignettes from these efforts will be shown to discuss how studying cell-type specific translation within a brain circuit helps uncover novel schemas of neural translation. Finally work pertaining to aging changes in models of neurodevelopmental disorders will be discussed to explore how the same molecular defects can temporally regulate behavior and signaling throughout an animal’s lifespan.

Speaker Bio

:

Speaker

:

Swetha Gowrishankar, Associate Research Scientist,

Affiliation

:

Yale University School of Medicine

Venue

:

CNS Seminar Hall

Time

:

4:00 PM

Date

:

3 Nov 2017

Abstract

:

Lysosome-filled axonal swellings are a major, but poorly understood feature of Alzheimer’s disease amyloid plaques. It is not clear what causes these axonal lysosomes to accumulate at amyloid plaques or whether they contribute to the disease pathology.  Our previous characterization of these lysosomes at amyloid plaques led us to propose a model where these axonal lysosomes accumulate due to a local defect in their retrograde transport and maturation and represent pathologically meaningful sites of Aβ production [1]. To test this hypothesis, we developed mouse genetic strategies to alter axonal lysosome abundance and examine the impact on amyloid plaque pathology. To this end, we identified JNK-interacting protein-3 (JIP3) as a candidate for regulating axonal lysosome abundance and validated such a function through extensive cell biological characterization of JIP3 KO mouse neurons. These efforts revealed that JIP3 is an important regulator of the transport, abundance and maturation state of axonal lysosomes. Furthermore, we observed multiple similarities between the axonal lysosomes that accumulate in JIP3 KO neurons and those that build up around amyloid plaques. This includes a build up of amyloid precursor protein (APP), and its processing enzymes- β-secretase (BACE1) and presenilin 2 (PSEN2). We detected significantly elevated Aβ levels in the JIP3 KO neurons, consistent with the hypothesis that the build up of the above-mentioned proteins leads to increased processing of APP into Aβ peptides, in the accumulating axonal lysosomes. Finally, our examination of the in vivo relationship between JIP3-dependent axonal transport of lysosomes and amyloid plaque pathology revealed that loss of JIP3 was accompanied by an increase in soluble Aβ levels, amyloid plaque size, abundance and axonal dystrophy [2].  These results collectively support a model wherein efficient retrograde axonal lysosome transport and maturation acts as a negative regulator of APP processing and the development of amyloid plaque pathology.

References:

1. Gowrishankar S, Yuan P, Wu Y, Schrag M, Paradise S, Grutzendler J, De Camilli P, Ferguson SM. 2015. Massive accumulation of luminal protease-deficient axonal lysosomes at Alzheimer’s disease amyloid plaques. Proc Natl Acad Sci U S A 112: E3699-708.

2. Gowrishankar S, Wu Y, Ferguson SM. 2017. Impaired JIP3-dependent axonal lysosome transport promotes amyloid plaque pathology. J Cell Biol.

Speaker Bio

:

Swetha received her Ph.D. in Cell Biology, from the laboratory of Prof. Satyajit Mayor, National Centre for Biological Sciences, Bengaluru in 2012.  As a graduate student she was the recipient of a CSIR-UGC fellowship (2006-2011).  Additionally, in graduate school she received a “Utrecht University Short stay fellowship” (a competitive 3-month fellowship awarded to carry out research at Utrecht University) that she utilized to learn cryo-immuno electron microscopy in the laboratory of Prof. Judith Klumperman at UMC, Utrecht. Since June 2013 she has been working as a post-doctoral fellow at Yale School of Medicine, in the laboratories of Prof. Pietro De Camilli and Prof. Shawn Ferguson. She received the Brightfocus Post-doctoral fellowship for research on Alzheimer’s disease (2016-2018), an international and highly competitive grant for research on Alzheimer’s disease, glaucoma or macular degeneration. As a post-doc she has been studying the cell biological mechanisms underlying Alzheimer’s disease pathology with a specific focus on lysosome transport and its role in the disease. Her work has helped shed light on a robust but poorly understood phenotype of Alzheimer’s disease-the accumulation of lysosomes in swollen axons around amyloid plaques. She is a member of American Society for Cell Biology (2006, 2010, 2013-current) and is also an active participant and post-doctoral mentor in the WISAY (Women in Science at Yale) program (2013-current).

Speaker

:

Sarika Cherodath, PhD,

Affiliation

:

National Brain Research Center, Gurgaon

Venue

:

CNS Seminar Hall

Time

:

4pm

Date

:

3 Nov 2017

Abstract

:

As opposed to language which is a skill human brain is biologically built for, the human brain does not have a dedicated region which helps it to read. Instead it adapts itself and builds a network of brain regions, originally intended to do other primary functions, to build a “reading network”. Since the advent of functional brain imaging, much has been revealed about this reading network in the brain in individuals learning a single language. However, a large majority of the world’s population grows up in environments, where they learn to read more than one language, often written in different scripts. However, the mechanism by which a child’s brain accomplishes reading in two languages, which often, are very distinct in its features and rules was largely unknown. Understanding the cognitive challenges faced by a developing reader in such a biliterate setting, is vital to further understand the brain basis of reading disabilities such as Dyslexia, as well as to refine educational policies in such a way as to better equip these children to face the challenges posed by the two or three-language educational policies set in several countries such as India. The study under discussion, aimed at understanding these brain mechanisms of reading by studying brains of 8-10 year old Indian children simultaneously learning to read Hindi and English in school, using a variety of methods such as structural and functional neuroimaging as well as behavioural measures of language and reading skills. The findings from the experiments have crucial implications on the understanding how brain networks are organized in children raised in biliterate learning environments and also establish normative data on typical reading networks in Hindi-English biliterates, paving way for future studies to explore neurobiological basis of reading disability in such settings.

Speaker Bio

:

I joined National Brain Research Centre after securing my B.Sc in Biotechnology from Bharathiar University. I went on to complete my Masters and Ph.D degrees in Neuroscience from NBRC, where my work dealt with exploring reading mechanisms in children who are raised as biliterate, in educational setting typical of India, where I studied Hindi-English biliterate children in particular. I have since worked as a postdoctoral research fellow at National Central University in Taiwan, where I worked on statistical learning skills and its link with language learning ability in bilingual readers of Mandarin.

Speaker

:

Dr. Vishal Kapoor

Affiliation

:

Max Planck Institute for Biological Cybernetics, Tuebingen

Venue

:

CNS Seminar Hall

Time

:

12:00 PM

Date

:

24 Oct 2017

Abstract

:

Multistable visual phenomena, wherein unchanging sensory input elicits in an observer, perceptual fluctuations, have been instrumental in unraveling the neural correlates of conscious perception. Such paradigms, when combined with single unit recordings in macaques trained to report their percept, have allowed neurophysiologists to elucidate, if the cells in various regions of the brain are correlated with subjective experience or respond to the invariant retinal input. Results obtained from such an approach have so far revealed that the proportion of feature selective cells which fire in concordance with perception, increase as one progresses in the ventral visual pathway, with this fraction being up to 90% in the temporal lobe. We have previously demonstrated the presence of perceptually modulated spiking activity in the lateral prefrontal cortex in a variant of the binocular rivalry paradigm called the binocular flash suppression. Recently, the role of lateral prefrontal cortex in conscious visual perception has been questioned for the very reason it was formerly proposed, that is its concomitant function of mediating task relevant behavior and motor action. Additionally, theoretical approaches on studying consciousness have cautioned on distilling the true correlates of consciousness from those related to its prerequisites and consequences. An fMRI study, utilizing a no-report binocular rivalry paradigm concluded that the bulk of frontal activity elicited during rivalry can be attributed to the motor report. In order to understand the neural activity during free flowing binocular rivalry, we recorded with multi-electrode Utah arrays from the ventrolateral prefrontal cortex of awake macaques engaged in a no report binocular rivalry paradigm. Analysis of spiking activity revealed robust modulations related to perceptual dominance and suppression in several recording sites. These findings indicate that perceptual content is represented in the spiking activity in the lateral prefrontal cortex, reinstating the existence of neural correlates of the conscious percept in this region of the primate brain.

Speaker Bio

:

Speaker

:

Dr. Suneel Reddy-Alla

Affiliation

:

Venue

:

CNS Seminar Hall

Time

:

10:00 AM

Date

:

16 Oct 2017

Abstract

:

Heterogeneity in synapse structure and function across neural circuits and different

regions of the brain is commonly observed phenomena. Synapses tend to undergo

depression or facilitation upon repetitive action and are tuned to function optimally at

certain frequency of neuronal activation. The molecular players involved in synaptic

transmission are currently being elucidated however how the functional differences arise

across different synapses remains unknown. To investigate on this I have studied on how

patterned formations of molecules important for SV fusion on the presynaptic plasma

membrane influence the functional properties of synapses through super-resolution

microscopy and electrophysiology. The results indicate that short plasticity and the

number of neurotransmitter release sites and their release probability are critically

determined by placement of active zone proteins and synaptic vesicle fusion machinery

relative to Ca+2 channels present at the center of synapse.

Speaker Bio

:

Speaker

:

Dr. Ramesh Kandimalla, Assistant Professor,

Affiliation

:

Garrison Institute of Aging, Texas Tech University

Venue

:

CNS Seminar Hall

Time

:

11:30 AM

Date

:

9 Oct 2017

Abstract

:

Previous studies in fungal models have reported that reducing mitochondrial fission can extend lifespan. Mitochondria dynamically change their shape by repeated fission and fusion in response to physiological and pathological conditions. Recent studies have uncovered significant roles of mitochondrial fission and fusion (such as mitochondrial dynamics) in neuronal functions, and auto/mitophagy and spine formation. Critically, however, the interplay between mitochondrial dynamics and mitophagy during aging remains poorly understood. However, the contribution of mitochondrial fission to the development of dendrites remains controversial. Here, we show that partial reduction of mitochondrial division protein Drp1—a Dynamin-related protein that inhibits the formation of phosphorylated Tau, amyloid beta (Aβ), mitochondrial abnormalities, the loss of dendritic spines, cognitive decline, and auto/mitophagy mechanisms [LC3, ATG5 PINK1 & TERT] in TauXDrp1+/− & APPXDrp1 +/- double mutant mice. Our findings in APP and Tau mice indicate that partial reduction of mitochondrial fission could delay the onset of Alzheimer’s disease pathology and mortality.

Speaker Bio

:

Speaker

:

Programme

Affiliation

:

Venue

:

ECE Golden Jubilee Hall, IISc

Time

:

09:30 AM - 04:00 PM

Date

:

4 Oct 2017

Abstract

:

Speaker Bio

:

Speaker

:

Dr. Deepika Suri

Affiliation

:

Columbia University, New York.

Venue

:

CNS Seminar Hall

Time

:

04:00 pm

Date

:

3 Oct 2017

Abstract

:

Adolescence constitutes a vulnerable period in humans, associated with the emergence of a range of psychiatric disorders including substance abuse. This period also coincides with the development of the dopaminergic reward circuit both in humans and in rodent systems. However, despite the wide prevalence of adolescent use of recreational drugs, several of which target the dopaminergic circuit, relatively little is known about their impact on the developing circuits and on adult neurophysiology and behavior. Using rodents models my research has identified that enhancing dopamine levels, in a narrow developmental window period in adolescence, increases adult dopaminergic circuit activity. We find that adolescent dopaminergic perturbations are also associated with enhanced aggression, potentiated behavioral responses to drugs of abuse and increased impulsive behavior in adulthood. Our findings from optogenetic manipulation and fiber photometric analysis of dopaminergic circuit activity demonstrate a causal relationship between dopaminergic hyperactivity and impulsive behavior. Current studies are using optogenetic inhibition to rescue the impulse dyregulation evoked in response to adolescent dopaminergic perturbation, and map the target regions that may be responsible for impaired impulse control.

Our results provide compelling evidence for the long term adverse effects of adolescent exposure to dopaminergic perturbations, and give a mechanistic understanding of the role of dopaminergic activity in impulse control psychopathology

Speaker Bio

:

Speaker

:

Prof. Kobi Rosenblum

Affiliation

:

University of Haifa, Sagol Department of Neurobiology

Venue

:

CNS Seminar Hall

Time

:

4:00 PM

Date

:

25 Sep 2017

Abstract

:

In the past decade we have aimed at dissecting out cortical molecular and cellular processes underlying different phases of simple forms of incidental (positive) as well as associative (negative) taste learning paradigms. We have identified time-dependent transcriptional, translational, and post translational modifications that are correlated and/or necessary for different forms or phases of taste learning. Currently, we aim at better understanding the relationships between the different molecular processes and their localization within the relevant cortical circuit underlying taste behavior. In addition, following the identification of new pathways and molecular targets to enhance cognitive function, we are testing the possibility that pharmacological or genetic manipulation of the newly identified pathways could ameliorate memory impairments in normal aging or rodent models of neurodegenerative diseases. One example for such pathway is the role of eIF2a and its kinases, GCN2, PKR, PERK in memory consolidation and sporadic Alzheimer disease.

Speaker Bio

:

Speaker

:

Sridevi V. Sarma, Ph.D., Assistant Professor,

Affiliation

:

Institute of Computational Medicine, Department of Biomedical Engineering, Johns Hopkins University, MD 21218

Venue

:

CNS Seminar Hall

Time

:

4:00 PM

Date

:

18 Sep 2017

Abstract

:

Decision-making links cognition to behavior and is a key driver of human
personality, fundamental for survival, and essential for our ability to
learn and adapt. It has been well established that humans make logical
decisions where they, for example, maximize an expected reward, but this
rationality is influenced by internal biases such as emotions. Psychiatric
patients who have dysfunctional cognitive and emotional circuitry
frequently make irrational decisions. Unfortunately, the function of
relevant neural circuits in humans is largely uncharted at fine temporal
scales, severely limiting the understanding of changes underlying
disruption associated with diseases. In this study, we localize neural
populations, circuits, and their temporal patterns on a millisecond scale
that are critically involved in human decision-making.

Twelve human subjects, implanted with multiple depth electrodes for
clinical purposes, performed a gambling task while we recorded local field
potential activity from deep and peripheral brain structures. The gambling
task consisted of a game of “high card”, where the subject bets high
($20) or low ($5) on whether her card will be higher than the computer’s
card. We posited that each subject’s decision-making system consists of
a feedforward model with the playing card as the input and betting
behavior as the output (e.g. how she bets and how quickly she bets). The
behavior and gambling outcome is a feedback signal to the model, which
updates an internal latent state (e.g. internal bias) of the feedforward
model. For each subject, we estimated the closed-loop decision making
system from betting behavior using maximum likelihood methods.

The models capture the variability amongst subjects and suggest a spectrum
of decision-makers that range from irrational to logical. Analysis of the
neural data suggest that particular oscillations in populations of neurons
of key limbic (amygdala, anterior cingulate cortex) and cognitive
structures (orbitofrontal cortex) encode different components of the
decision-making system such as the expected reward and risk of reward.
These findings provide new insight into how humans link their internal
biases (e.g. emotions) with logic to make decisions.

Speaker Bio

:

Sridevi Sarma received the B.S. degree in electrical engineering from
Cornell University, Ithaca NY, in 1994; and an M.S.  and Ph.D. degrees in
Electrical Engineering and Computer Science from Massachusetts Institute
of Technology in, Cambridge MA, in 1997 and 2006, respectively. From
2000-2003 she took a leave of absence to start a data analytics company.
From 2006–2009, she was a Postdoctoral Fellow in the Brain and Cognitive
Sciences Department at the Massachusetts Institute of Technology,
Cambridge. She is now an associate professor in the Institute for
Computational Medicine, Department of Biomedical Engineering, at Johns
Hopkins University, Baltimore MD. Her research interests include modeling,
estimation and control of neural systems using electrical stimulation. She
is a recipient of the GE faculty for the future scholarship, a National
Science Foundation graduate research fellow, a L’Oreal For Women in
Science fellow, the Burroughs Wellcome Fund Careers at the Scientific
Interface Award, the Krishna Kumar New Investigator Award from the North
American Neuromodulation Society, and a recipient of the Presidential
Early Career Award for Scientists and Engineers (PECASE) and the Whiting
School of Engineering Robert B. Pond Excellence in Teaching Award.

Speaker

:

Dr. Achira Roy Ph.D.

Affiliation

:

Center for Integrative Brain Research, Seattle Children’s Research Institute Seattle, WA, USA

Venue

:

CNS Seminar Hall

Time

:

3:00 PM

Date

:

12 Sep 2017

Abstract

:

Speaker Bio

:

Speaker

:

Dr. Marieke van Vugt, Assistant Professor,

Affiliation

:

Institute of Artificial Intelligence and Cognitive Engineering, University of Groningen, Netherlands

Venue

:

CNS Seminar Hall

Time

:

4pm

Date

:

18 Aug 2017

Abstract

:

Speaker Bio

:

Speaker

:

Dr. Kunjumon Vadakkan, Scientist,

Affiliation

:

Neurosearch Center, 76 Henry Street,
Toronto, Ontario, Canada, M5T 1X2

Venue

:

CNS Seminar Hall

Time

:

3pm

Date

:

11 Aug 2017

Abstract

:

Camillo Golgi developed the Golgi technique. But he had severe difficulties in agreeing with the Neuron doctrine, which is  evident by reading his Nobel Prize lecture. Even though no one could  really understand the reason for his disagreements until now, there  was no need to undertake experiments to examine Golgi‘s view. Here, I  will present some preliminary neurobiological evidence to suggest why  Golgi disagreed with the Neuron doctrine. I will discuss the implications of these findings in the future research.

Speaker Bio

:

Speaker

:

Dr. Sadique Sheik

Affiliation

:

BioCircuits Institute, UCSD

Venue

:

CNS Seminar Hall

Time

:

3:00 PM

Date

:

2 Aug 2017

Abstract

:

Spiking neural networks can be used to construct computational machines
such as RBMs. More recently, SSMs were shown to outperform equivalent
ac{RBM}s. SSMs with stochastic synapses implemented in FPGA-based
spiking neural networks can obtain a high accuracy in classifying MNIST
handwritten digit database. In the first part of the talk I argue that
stochastic synapses have the same effect as synapses with higher bit
precision but require significantly lower computational resources. This
paves way to exploration of Spiking Neural Networks for unsupervised
machine learning applications.

Several learning rules for synaptic plasticity, that depend on either
spike timing or internal state variables, have been proposed in the
past, imparting varying computational capabilities to Spiking Neural
Networks. Some of the key capabilities that the spiking neurons are
particularly suited for and efficient at is the ability to recognize
complex spatial and temporal correlations in their inputs. While such SNNs
would ideally benefit from specialized neuromorphic hardware
implementations for low-power real-time computations, the complexity of
learning rules prohibits or limits hardware implementations. But due to
design complications these learning rules are typically not implemented on
neuromorphic devices leaving the devices to be only capable of inference.

In the second half of the talk I introduce a unidirectional post-synaptic
potential dependent learning rule that is only triggered by pre-synaptic
spikes, and easy to implement on hardware. We demonstrate that such a
learning rule is functionally capable of replicating computational
capabilities of pairwise STDP. Further more, we demonstrate that this
learning rule can be used to learn and classify
spatio-temporal spike patterns in an unsupervised manner using individual
neurons. We argue that this learning rule is computationally powerful and
also ideal for hardware implementations due to it’s unidirectional memory
access. Finally I present results showing that
neurons can learn to differentiate between various dynamic human gestures
upon exposure spikes directly recorded from spiking vision sensors.

Speaker Bio

:

Sadique Sheik received his BSc, MSc in Physics from IIT Kharagpur in
2007. After a brief period with IBM India he started his PhD at Institute
of Neuroinformatics, ETH Zurich and graduated in 2013. He moved to UCSD to
as a Post-Doc to continue his research at the BioCircuits Institute. His
research focuses on online learning rules for spiking neural networks and dynamical systems.
He is interested in developing cognitive computational models that are optimal for
neuromorphic implementations, asynchronous event based computation and
designing neuromorphic architectures for optimal computation.

Speaker

:

Aditya Gilra

Affiliation

:

Computational Neuroscience Laboratory (IC/SV), CH-1015 Lausanne, Switzerland

Venue

:

CNS Seminar Hall

Time

:

4:00 PM

Date

:

1 Aug 2017

Abstract

:

To plan and control movement, the brain must construct a model of
the non-linear dynamics of the body in response to neuro-muscular
commands. How a network of spiking neurons (in the brain) can learn such a
model, by adjusting interconnection weights in a biologically plausible
way, is still unresolved. As an advance in this direction, we propose a
local and stable learning scheme, Feedback-based Online Local Learning Of
Weights (FOLLOW) [Gilra and Gerstner,arXiv:1702.06463]. We show that the
learning scheme is uniformly stable with the error going to zero
asymptotically, under reasonable approximations. We apply the FOLLOW
scheme to enable a network of interconnected spiking neurons to learn the
dynamics of a linear, non-linear or chaotic example system. We also make
the network learn the dynamics of a simplified two-link arm, then use the
network to control the arm, to draw a desired shape on a wall. Ongoing
extensions will also be discussed.

Speaker Bio

:

Speaker

:

Dr. Arjun Ramakrishnan

Affiliation

:

University of Pennsylvania

Venue

:

CNS SEMINAR HALL

Time

:

04.00 PM

Date

:

29 May 2017

Abstract

:

Sensitivity to reward is a fundamental mechanism that allows living
organisms to navigate in an ever-changing environment. Severe changes in
reward sensitivity has been, in fact, associated with many mental health
conditions like depression and bipolar disorder. To understand how reward
– be it in the form of food or social stimuli – influences action planning
and decision making, I have looked  at the representation of reward in
sensorimotor brain areas of non-human primates. These studies for the
first time revealed neurons that co-represent reward expectation along
with movement kinematics in their activity, implicating primary motor
areas in reward-based learning mechanisms. Considering the paramount role
of reward in influencing our actions, I have recently developed an
ecologically relevant, mathematically tractable, explore-exploit
decision-making paradigm. By deploying the task in conjunction with
various non-invasive measures like EEG, pupillometry and blink rate, I
hope to establish neural biomarkers for depression and other mental health
conditions.

Speaker Bio

:

Speaker

:

Rashmi Gupta, PhD.

Affiliation

:

Postdoctoral fellow,
Swiss Center for Affective Sciences,
University of Geneva, Switzerland

Venue

:

CNS SEMINAR HALL

Time

:

11.30 AM

Date

:

9 May 2017

Abstract

:

Many emotional distractors surround us in our daily life. For
example, emotional faces, beautifuL buildings, accident scenes and so
on. It is very important to ignore these emotional distractors in
order to perform in a primary task in hand. In my research I asked
what is the role of attention in our ability to ignore emotional
distractors. Role of attention in positive distractor processing is
unknown. I argued that to get a complete picture of emotion processing, it
is very important to study positive distractors by directly comparing it
to negative distractors. To test this, I performed series of experiments
using behavioural, eye-tracker, functional magnetic resonance imaging
(fMRI) and Electroencephalography (EEG) methods. I found that it is easier
to ignore negative images (angry faces, sad faces, mutilated bodies, faces
associated with punishment) than positive ones (happy faces, faces
associated with reward, erotic pictures) when focusing on other things
(Gupta et al., 2016; Gupta & Srinivasan, 2015). This effect was paralleled
by another study that showed that irrelevant happy faces are better
recognized than sad faces under conditions of distributed attention. The
study provides evidence that attentional “style” (focused or distributed
attention) interacts with the emotional content of stimuli in a scene to
determine subsequent memory for that scene (Gupta & Srinivasan, 2015;
Srinivasan & Gupta, 2010; Srinivasan & Gupta, 2011). Other set of
experiments showed that the processing of emotional and high motivational
salient (high value learned) distractors is right hemisphere biased (Gupta
& Raymond, 2012). Using functional magnetic resonance imaging (fMRI)
method, I found that the high motivational salient faces (relative to low
motivational salient faces) activated the primary visual cortex of the
brain more even they were invisible (unconscious) to observer (Gupta et
al., manuscript under preparation, data collected and analyzed). These
findings have implications in psychological well-being, consumer
psychology, marketing and advertisements.

Speaker Bio

:

Dr. Rashmi Gupta is a Cognitive Neuroscientist. She is an expert in
Experimental Cognitive Psychology. She conducted research on various
research topics such as cognition and emotion, value, motivation,
attention, memory, perception, cognitive disorders and child development.
She received undergraduate degree in Psychology and masters
& PhD in Cognitive Sciences from the Centre of Behavioural and Cognitive
Sciences (CBCS), University of Allahabad. Rashmi Gupta was the first
person to receive a PhD degree in Cognitive Sciences in India. She
worked with renowned scientist in the filed at various universities
across the world. She has worked at the Bangor University, UK,
University of California San Diego, USA, University College London (UCL),
UK and the University of Geneva (UNIGE), Switzerland. She received highly
prestigious and competitive research grants such as grants from the
International Brain Research Organization, Marie Curie Actions, National
Science Foundation and so on with funding amount of roughly six hundred
thousands Euros (nearly 5 Cr. INR). She published her research at various
leading journals like ‘Emotion,’ ‘Quarterly Journal of Experimental
Psychology’, ’‘Cognition
and Emotion’, ‘Psychonomic Bulletin and Review’, ‘Progress in
Brain Research’, ‘Frontiers in Psychology’ and others, in the field.
She is an associate editor for ‘Frontiers in Psychology’ journal and
an ad-hoc reviewer for multiple journals. She is an elected member of the
scientific committee of the University of Padova, Italy. She taught
several courses such as ‘Introduction to Psychology’, ‘Attention’,
‘Cognitive Disorders’, and ‘Research and
Methods’ at CBCS, UCL, and UNIGE. She supervised four masters, one
undergraduate and two interns for their theses. All her students
received ‘first class grade’ on their theses and they all are now
pursuing their PhDs at universities across the world. Rashmi was awarded
as one of the top-ten one-minute TEDx speakers at TEDx-CERN Geneva
competition. She maintains more than 20 international collaborations. Also
she has developed various tools such as ‘Indian face database’,
‘computer based classification system’, and rehabilitation program for
ADHD children’ that has contributed to research community.

Speaker

:

Dr.Ayan Sengupta,

Affiliation

:

Postdoctoral Research Fellow in Sir Peter Mansfield Imaging Center, University of Nottingham, UK.

Venue

:

CNS Seminar Hall

Time

:

4:00 PM