Seminars

Speaker

:

Dr. Sivakumar Sambandan

Affiliation

:

Synaptic Metal Ion Dynamics and Signaling, Laboratory of Neurobiology, MPI for Multidisciplinary Sciences, Göttingen, Germany

Venue

:

CNS Seminar Hall

Time

:

12.00 PM

Date

:

23 Dec 2022

Abstract

:

The importance of zinc in the health of immune system is well established. However, the role of zinc in the function of nervous system is poorly understood although it is known for several decades that zinc is highly enriched at neuronal synapses. We recently found that synaptic vesicles that co-store glutamate and zinc are the most abundant vesicles in the brain, and that zinc facilitates the vesicular glutamate content and postsynaptic quantal size. During the talk, I will discuss the molecular mechanism by which zinc effects the regulation of glutamate mediated synaptic excitation. In addition, I will dwell on a novel and powerful super resolution technique, Minflux 3D nanoscopy, to deduce the ultrastructure of glutamatergic synapses with molecular specificity. The 3D resolution at the nanoscale level reveals unprecedented insights on the intrasynaptic organization of different vesicle pools at individual synapses. Using the above quantitative data, I will try to compare the capacity of the zincergic system that is spatio-temporally locked with glutamate release to modulate neuronal excitation with that of the inhibitory circuit mediated by GABA through a separate population of neurons. Considering the vast abundance of glutamate-zinc vesicles, zinc action could underlie a systemic and robust mechanism to modulate neuronal excitation.

Speaker Bio

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Speaker

:

Dr. Abhilasha Joshi

Affiliation

:

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

15 Dec 2022

Abstract

:

As animals move in complex environments, higher-order cognitive computations in the hippocampus—a brain region critical for navigation—reflect an internal map of the external world. This map is represented by the firing of single neurons at specific locations in the environment (i.e., place cells) and the population activity rhythmically fluctuating at ~8Hz. Thus, during navigation, hippocampal neural activity corresponds to rhythmic and sequential spatial representations at, behind, or ahead of the actual location of the animal. The act of navigation, in turn, critically depends on locomotion; however, current accounts suggest a dissociation between hippocampal spatial representations and the details of locomotor processes. In my postdoctoral work, I evaluated the possibility that hippocampal spatial representations and ongoing steps are synchronized with each other by simultaneously monitoring them at fast timescales during behaviour. We have found that the forelimb stepping cycle in freely behaving rats is rhythmic and peaks at ~8 Hz during movement, matching the ~8 Hz organization of information processing in the hippocampus during locomotion. We also discovered a precisely timed coordination between the time at which the forelimbs touch the ground (‘plant‘ times of the stepping cycle) and the hippocampal representation of space. Notably, plant times coincided with hippocampal representations closest to the actual position of the animal, while in-between these plant times, the hippocampal representation progressed toward possible future locations in the behavioural arena. This synchronization was specifically detectable when animals approached upcoming spatial decisions. Taken together, our results reveal a dynamic coordination on a timescale of tens of milliseconds between central cognitive representations and peripheral motor processes. This coordination engages and disengages rapidly in association with cognitive demands and is well suited to support rapid information exchange between cognitive and sensory-motor circuits.

Speaker Bio

:

Simons Collaboration on Plasticity and the Aging Brain Transition to Independence fellow,
Howard Hughes Medical Institute Fellow of the Life Sciences Research Foundation,
Departments of Physiology and Psychiatry, University of California, San Francisco, California

Speaker

:

Dr. Arnab Barik

Affiliation

:

Assistant Professor, CNS, IISc

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

14 Dec 2022

Abstract

:

Speaker Bio

:

Speaker

:

Thangaraj Senthil Kumar

Affiliation

:

EPFL, Lausanne, Switzerland

Venue

:

CNS Seminar Hall

Time

:

12.00 PM

Date

:

2 Dec 2022

Abstract

:

Neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), and frontotemporal lobar degeneration (FTLD) are fatal but clinically distinctive disorders. These diseases, in common, are pathologically characterized by the presence of abnormal aggregation of one or many cellular proteins in different cell types, thus exhibiting different distributions of neurodegeneration. For example, TDP-43 in ALS/FTLD and a-synuclein in PD are the proteins that undergo aberrant aggregation. Enormous efforts have been underway to investigate the structure and formation of these pathological aggregates in vitro and in pre-clinical cellular models to understand the associated disease mechanisms and ultimately to develop novel strategies for diagnostic and therapeutic purposes. To gain insight into these, in my post-doctoral work, we worked on aims that employed multi-disciplinary approaches from structural biology to cell biology. In this presentation, I will talk about: 1) the knowledge that we gained on the sequence and structural determinants of TDP-43 aggregation and its proteolytic events that might lead to its neurotoxicity in ALS/FTLD1 ; 2) the efforts that we made for the development of the methods and tools for advancing research and drug discovery efforts in PD and other synucleinopathies2- 4 . Finally, I will also discuss how our current findings raise important questions that set the basis for my future research objectives.

Speaker Bio

:

Speaker

:

Dr. Swagata Dey

Affiliation

:

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

1 Dec 2022

Abstract

:

Speaker Bio

:

Speaker

:

Eric Hosy

Affiliation

:

Director of Research, IINS, CNRS-Université de Bordeaux. Bordeaux, France

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

23 Nov 2022

Abstract

:

The synapse is a 1 µm size bi-partite organelle responsible of the talk between neurons. The role of glutamate receptors is to convert the chemical signal emits by the pre-synapse (glutamate release) to an electrical signal understandable by the post-synaptic neuron. Due to their relatively low affinity for glutamate and to the limited amount of glutamate, the spatiotemporal nano-organization of these receptors in post-synaptic membrane is fundamental to understand synaptic transmission and so information processing by the brain. This nanoscale sub-synaptic organization has been rendered accessible by the use of single particle based super-resolution microscopy. By combining these techniques with electrophysiology and modeling, we succeeded to improve our tight understanding of synaptic transmission properties. Through this seminar we will revisit at the nanoscale the basics of synaptic transmission from a glutamate receptor side.

Speaker Bio

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Speaker

:

Prof. Ramakrishnan A. G.

Affiliation

:

MILE Lab, Dept of Electrical Engineering, Associate faculty, CNS

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

22 Nov 2022

Abstract

:

The electrical activity of the brain, the key control organ of our body, carries a lot of information about our current activity, health, mental status, and identity. We, in MILE Lab, have been focussing for the past few years on analyzing the various patterns present in the electroencephalogram (EEG). When someone is in deep sleep, coma, or under anesthesia, the level of consciousness is lower than that of the waking state. When someone has locked-in syndrome, the level of consciousness is the same as that of the waking state. On the other hand, during meditation, the consciousness level is higher than that of waking. Hypnosis is another completely different altered state of consciousness. The interrelationship between the different EEG channels is also distinctly different during inhalation, breath-hold after inhalation, exhalation, and breath-hold after exhalation. We are studying the patterns in EEG under all the above conditions. While working on the above topics, we unexpectedly made a discovery that some measures based on the functional connectivity between the channels are distinct for each individual and can very well be used to identify people. Using other measures, we are also able to predict the word imagined by a person out of a set of words.

Speaker Bio

:

Speaker

:

Dr. Mini Jose Deepak

Affiliation

:

Ramalingaswami Fellow

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

16 Nov 2022

Abstract

:

Cholesterol regulation and homeostasis in the brain is a fundamental requirement for health. Alteration in lipid homeostasis is thought to be causal for many neurodegenerative and developmental disorders. Recent studies from our lab signifies the importance of membrane cholesterol balance in determining neuronal development and architecture. Neurons have a unique structure with a singular axon and multiple dendrites, which makes it not only one of the most beautiful cells in the brain, but also compliments its unique function in forming the extended wiring within the brain. Neuronal polarization plays a critical role in determining the neuronal architecture which is generated by the interplay of molecular feed-back loops, differential localization of polarity effectors and effector cytoskeletal molecules. Though the lipid balance and compositionality of the membrane are thought to be critical in neurite outgrowth, the fine regulation of membrane cholesterol on the axonal and dendritic development particularly at very early stages, from the initiation of protrusions to breaking of symmetry and polarity establishment, has never been explored in detail. Recent evidence from our lab is one of the first which signifies the stark effect of a transient alteration in membrane cholesterol balance, resulting in long term deficits on neurite outgrowth and polarity establishment. Our study also emphasizes the importance of addressing this condition at an early developmental phase when the deficits can be rescued by precise control of the lipid membrane balance.  We also pursue challenging attempts to rescue the developmental defects observed on cholesterol sequestering by co-modulating multiple key players in alternative pathways. Our lab also focusses on the role of cAMP mediated second messenger pathways in controlling neuronal polarity. Combining optogenetics with super resolution microscopy, we showed how photoactivation of adenylyl cyclases control the stochastic organization and lateral diffusion of HCN channels involved in regulating neuronal membrane potential. Together, we try to understand the different signalling pathways regulating neuronal development and polarity establishment. 

Speaker Bio

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Speaker

:

Dr. Vivek Kumar

Affiliation

:

Associate Professor, The Jackson Laboratory

Venue

:

CNS Seminar Hall

Time

:

11:00 AM

Date

:

11 Nov 2022

Abstract

:

Speaker Bio

:

Speaker

:

Dr. Deependra Kumar

Affiliation

:

International Institute for Integrative Sleep Medicine (IIIS), University of Tsukuba, Japan

Venue

:

CNS seminar hall, ground floor.

Time

:

11.30 AM

Date

:

9 Nov 2022

Abstract

:

The occurrence of dreaming during rapid eye movement (REM) sleep prompts interest in the role of REM sleep in hippocampal-dependent episodic memory. We found that the sparse activity of hippocampal adult-born neurons (ABNs) during REM sleep is necessary for memory consolidation (Kumar et al., Neuron 2020). The number of ABNs correlates with the strength and persistence of memory. Also,  young ABNs neurons show enhanced synaptic plasticity compared with their fully mature counterpart and may be preferentially recruited into a memory trace. So, we imaged the activity of young ABNs during contextual fear conditioning and subsequent REM sleep. ABNs active after learning reactivate in the next REM sleep. Optogenetic manipulation of ABNs activity in REM sleep impairs memory consolidation. 

REM sleep and hippocampal ABNs are high during infancy, although freshly generated memories are rapidly forgotten (infantile Amnesia). My current research explores the critical age of development when REM sleep and ABNs participate in the memory consolidation mechanism. The dreamless is the suitable mice model for this study because they sleep less in REM sleep (Funato et al., Nature 2016).

Speaker Bio

:

Speaker

:

Dr. Supriya Ghosh

Affiliation

:

Department of Neurobiology, The University of Chicago

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

17 Oct 2022

Abstract

:

Attention greatly improves behavioral performance. Although there are many different aspects of attention as defined in psychology, the underlying neuronal mechanisms remain poorly defined. Two fundamental aspects of attention, selectivity and cognitive effort–how intensely attention is focused– are considered to be independent processes in psychophysical theories. In recordings from individual neurons while monkeys’ spatially selective attention and effort at two locations were independently controlled, we found that neuronal activity in visual area V4 is robustly modulated by either selective attention or effort. Notably, increasing overall effort to improve performance at a distant site reduced neuronal responses even when performance was unchanged for receptive field stimuli. This interaction between attentional selectivity and effort can be explained by divisive normalization of spatially distributed behavioral performance. To further delineate neurobiological substrates of attention, we optogenetically activated specifically norepinephrine (NE) neurons in the locus coeruleus (LC) while monkeys were performing visual attention tasks. We found that the spiking of LC-NE neurons shows strong, spatially-selective attention-related modulation, and demonstrate that optogenetically enhancing the spiking of LC-NE neurons robustly improves behavioral detection for visual stimuli contralateral to the stimulated LC. These results suggest a selective contribution of NE neuromodulation to attention-related behavioral enhancements beyond its widely thought of role in non-selective form of arousal.

Speaker Bio

:

Speaker

:

Dr. Preeya Khanna

Affiliation

:

Dept. of Neurology
University of California, San Francisco

Venue

:

CNS seminar hall, ground floor.

Time

:

04.00 PM

Date

:

6 Oct 2022

Abstract

:

In today’s society, we cannot live independently without the use of our hands. We flexibly use our hands to eat, to type messages, and to work for a living. This reality makes damage to the neural circuits controlling hand function in stroke, spinal cord injury, and other neurological injury patients especially devastating. In this talk I will focus on advances in characterizing and modeling motor cortical activity dynamics that support fast, successful upper limb movements, and how these advances have laid the foundation for neural interface technologies that can restore and rehabilitate function following stroke. I will describe results from a preclinical neuromodulation study and clinical brain-machine interface study that restored and rehabilitated upper limb function, presenting a promising future for neurophysiologically-inspired neural interfaces. Finally, I will discuss future directions in simultaneously monitoring and modeling the motor and somatosensory neural components of hand movements during realistic object manipulation tasks towards next-generation neural interfaces that can reinstate the dexterity needed to independently eat, type, and work.

Speaker Bio

:

Speaker

:

Prof. S P Arun

Affiliation

:

Professor & Chair, CNS, IISc

Venue

:

CNS Seminar Hall

Time

:

04.00 PM

Date

:

14 Sep 2022

Abstract

:

The adage “Old wine in a new bottle” illustrates the challenge of deciding if two items are same or different. Have I seen this person before? Are these two fruits identical? Are these two products identical? We make countless such choices each day, suggesting that the concept of same or different is a fundamental building block of cognition. This task would be trivial if there were no differences between items we need to call as same, and large differences between items that we need to call different. But this task is non-trivial because even the same object can look very different under different conditions, and related objects often share similarities and yet have differences.

How does the brain solve same-different tasks? Can we use the same-different task to understand vision and cognition? I will present some recent findings from our lab revealing the computations in the brain underlying the same-different task, and some ongoing work in which we are exploiting the versatility of this task to answer a variety of questions about visual perception.

Speaker Bio

:

Speaker

:

Dr. Saloni Sharma

Affiliation

:

Postdoctoral Fellow, Marge Livingstone lab, Harvard University

Venue

:

CNS Seminar Hall

Time

:

03.00 PM

Date

:

13 Sep 2022

Abstract

:

Face pareidolia refers to seeing an illusory face in inanimate objects. Emerging neuroimaging evidence suggests that face-selective regions in the primate ventral visual stream respond more to pareidolia compared to control objects (Taubert et al, 2022; Wardle et al, 2020). In this talk, I will demonstrate that although macaque face-selective neurons do show a stronger response for pareidolia images compared to matched control objects, the face-like configuration (or the perceived faceness) of the pareidolia images, which is critical for the perceptual experience of an illusory face, is not necessary to drive the responses of face-selective cells.

Speaker Bio

:

Speaker

:

Dr. Tanvi Deora

Affiliation

:

University of Washington, Seattle

Venue

:

CNS seminar hall, ground floor.

Time

:

04.00 PM

Date

:

1 Sep 2022

Abstract

:

From reaching and grasping to locomotion in complex habitats, movement control in biology demands feedback from a wide variety of sensors to orchestrate motor output. Importantly, the mechanics of sensory and motor structures condition sensory information and shape the motor control. My research focuses on insect-plant pollination interactions as a model to understand the interplay of sensing, actuation, and mechanics in driving emergent behaviors. As insects like moths and butterflies approach flowers, they uncoil their extremely long and flexible mouthpart, the proboscis and use it to probe the floral surface until they locate a tiny nectary hole and feed from it. Not only do they precisely locate a tiny target to feed from, but they do so while hovering, and with great rapidity as they move from flower to flower. The proboscis itself is a unique sensory structure: its motion is actively driven, and its mechanical properties are tunable. Understanding how insects like moths and butterflies expertly target a tiny hole will help us uncover general principles about how mechanics, sensing and actuation shape behaviors as well provide insights into the fundamental ecological process of pollination.

During my talk, I will briefly discuss my past research on the mechanical control of insect flight as well as the neural encoding by spatially distributed strain sensors on hawkmoth wings, both of which highlight the interplay between sensing and biomechanics. I will finally present my current work on tactile sensing in insect-plant pollination interactions that aims to understand how hawkmoths extract tactile cues from floral surfaces as well as the role of multimodal sensory feedback in movement control. My future work will draw upon a range of technological approaches including electrophysiology, computational neuroscience and machine learning & machine vision methods for behavioral analysis to pursue a research career that melds neurophysiology, mechanics, behavior, and ecology and provides insights into mechanisms of movement control in the natural world.

Speaker Bio

:

Speaker

:

Amrutha Swaminathan

Affiliation

:

Weizmann Institute of Science

Venue

:

CNS seminar hall, ground floor.

Time

:

04.00 PM

Date

:

23 Aug 2022

Abstract

:

Developmental processes influence individual health later in life. In my talk, I will discuss how major defects in development lead to neurological diseases, while subtle differences result in the establishment of individual behaviours.

I will first detail how we used a combination of behavioural and molecular biology tools to understand the mechanisms driving epileptogenesis. Specifically, we found a new role for an mTOR inhibitory factor, depdc5, in the formation of inhibitory neurons. The two processes, i.e., defective mTOR regulation and GABAergic neuron maturation independently lead to epilepsy when DEPDC5 is mutated.  In the second half of my talk, I will discuss my work on the ontogeny of stress resilience. Individuals in a population respond differently to stressful situations, with some being more resilient than others. However, it remains challenging to identify and study resilience early in life using mammalian embryos. I will discuss how I recently developed a high-throughput behavioural assay to identify subtle differences in stress-responsive behavior early during vertebrate development. Using this assay, we established that stress resilience is observed early in life as a stable and heritable trait. Using a combination of pharmacological and genetic tools, we found that this trait is regulated positively by neuropeptides and negatively by the innate immune complement system.

Speaker Bio

:

Speaker

:

Dr. Qiufu Ma

Affiliation

:

Professor at Harvard Neurobiology Department and Dana-Farber Cancer Institute

Venue

:

Video Conference

Time

:

05.00 PM

Date

:

28 Jul 2022

Abstract

:

Pain research currently faces a crisis, with few preclinical animal studies translating into new pain medicine. In this talk, Dr. Ma will discuss a new functional subdivision of the somatosensory system, from which he argues that preclinical studies might have been using behavioral assays that fail to measure clinically more relevant affective pain. He will then point out an even bigger challenge caused by the presence of redundant pain pathways, both at molecular and circuit levels. He will finally discuss on how electroacupuncture could be potentially used to eliminate the source such as inflammation that drives redundant pain pathways, via driving somato-autonomic neural pathways.

Speaker Bio

:

He received his BS from Fudan University in 1987 and PhD from UCLA in early 1994. After postdoctoral training at Caltech, he became an Assistant Professor at Harvard Neurobiology Department and Dana-Farber Cancer Institute, and then a full Professor in 2011. His lab has been working on the somatic sensory circuits, including somato-autonomic reflex pathways, as a way to understand how acupuncture works.

Speaker

:

Rajesh P. N. Rao

Affiliation

:

Hwang Professor of CSE and ECE at the University of Washington & Pratiksha Trust Visiting Chair Professor at IISc

Venue

:

CNS seminar hall, ground floor.

Time

:

04.00 PM

Date

:

25 Jul 2022

Abstract

:

I will present some recent results from my lab in the areas of brain-computer interfacing (BCI) and theoretical neuroscience. In BCI, I will present results on using backpropagation to train brain co-processor networks to restore grasping function after a simulated stroke in a computational model of sensorimotor cortex. In theoretical neuroscience, I will introduce dynamic and active predictive coding, two new theories of cortical function which extend the traditional model of predictive coding to hierarchical prediction of temporal sequences and sensorimotor behaviors.

Speaker Bio

:

Speaker

:

Prof. Anand Chandrasekhar

Affiliation

:

Professor in the division of biological sciences at the University of Missouri

Venue

:

CNS seminar hall, ground floor.

Time

:

11:00 AM

Date

:

21 Jul 2022

Abstract

:

Speaker Bio

:

The Professor in the division of biological sciences at the University of Missouri. He has MSc (biology) and B.Tech. (Electrical and electronics engg) from BITS Pilani, followed by a PhD from the University of Iowa. He followed that with a postdoctoral stint at the University of Michigan. He is a faculty member at the University of Missouri since 1999, where he works on developmental neurobiology, using zebrafish and mice, with strong interests in neural circuits and behavior.

Speaker

:

Dr. Vignesh Muralidharan

Affiliation

:

Postdoctoral Fellow
Aronlab of Cognitive Neuroscience
UCSD

Venue

:

Video Conference

Time

:

10.00AM

Date

:

15 Jul 2022

Abstract

:

In everyday life, we encounter situations where we need to control our actions, urges, thoughts, and emotions to achieve both short and long-term goals. For instance, one would have to control the urge to eat junk food while on a diet. One such form of executive control, referred to as inhibitory control, is the ability to stop or override unwanted actions and provocations from occurring, especially in situations where there is a strong pull toward them. There are different contexts where this form of control might be needed. In some scenarios, one might have to stop already initiated actions in reaction to external cues (reactive control), thus driving top-down control processes, e.g., stopping yourselves from stepping onto the street when you see a car rushing towards you. In other cases, one might have to prepare in advance and set up mental states that can aid in stopping (proactive control), e.g., stopping anxious thoughts before an important exam. Multiple lines of evidence have shown that such forms of inhibitory control of actions involve brain networks that include prefrontal, basal ganglia, and sensorimotor regions. In my talk, I will outline the ways in which we probed the neural correlates of control in these brain regions as people attempted to stop initiated actions or induced brain states that aided in stopping movements. I will also explain how our findings, using high temporal resolution electrophysiology, functional brain stimulation, and computational modeling approaches, revealed the dynamics of these regions and the role of specific brain (beta-band) rhythms while people exerted these forms of control. I will finally discuss how these findings form the precursors for future research aimed at developing strategies that can aid people’s ability to control their actions and thoughts. This research plan could potentially lead to applications that target behavioral deficits in impulse-control disorders like Parkinson’s disease, Tourette’s syndrome, obsessive-compulsive disorder, and anxiety-related disorders.

Speaker Bio

:

Speaker

:

T. Thippeswamy

Affiliation

:

BVsc, MVSc, PhD The Epilepsy Research Lab Professor, Biomedical Sciences College of Veterinary Medicine Iowa State University, Ames United States, IA 50011

Venue

:

CNS seminar hall, ground floor.

Time

:

04.00 PM

Date

:

12 Jul 2022

Abstract

:

Environmental neurotoxins such as organophosphate (OP) and domoic acid (DA) exposure can cause CNS disorders. The disorders range from neurobehavioral comorbidities/ dysfunction to the development of more severe diseases such as Parkinson’s, dementia, and epilepsy. OP is an ingredient in some pesticides and nerve agents. DA is a naturally occurring toxin produced by certain types of algae found on the West coast of California to Alaska in the Pacific Ocean. OP or DA can be fatal to humans if consumed in large quantities. Accidental or intentional acute exposure to OP/DA at a high dose causes status epilepticus (seizures for a prolonged period) and death if not treated immediately. The majority of the survivors in experimental models (>95%) develop epilepsy. The current antiepileptic or antiseizure drugs control seizures in 65% of people with epilepsy. However, these drugs do not mitigate brain pathology effectively though they manage symptoms, i.e., seizures. In the other 35%, the current medication has no effect. Therefore, identifying the targets that promote brain pathology in response to OP/DA-induced seizures can be potential novel therapeutic targets for the prevention or modification of the development of epilepsy/brain pathology. We have identified two novel targets (enzymes) in the experimental model of OP/DA; an inducible nitric oxide synthase (iNOS or NOSII) and a Src/Fyn tyrosine kinase. Our research demonstrates that targeting these enzymes with pharmacological inhibitors soon after the onset of OP/DA exposure in experimental models modifies the development of epilepsy (i.e., spontaneously recurring seizures, neuroinflammation, and neurodegeneration). The role of Fyn and its interaction with phosphorylated tau (pTau) as a target for disease-modification will also be discussed.

Speaker Bio

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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. Ofer Yizhar

Affiliation

:

Weizmann Institute Of Science

Venue

:

Video Conference

Time

:

04.00 PM

Date

:

31 May 2022

Abstract

:

Speaker Bio

:

Offer obtained his PhD from the Tel Aviv University, working on molecular mechanisms of synaptic transmission. He did his postdoctoral work at Stanford University between 2008-2011, and joined the Weizmann Institute in 2011.

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

:

Dr. Vignayanandam R. Muddapu

Affiliation

:

Postdoctoral Researcher, Blue Brain Project, EPFL

Venue

:

Video Conference

Time

:

04.00 PM

Date

:

28 Dec 2021

Abstract

:

Parkinson’s Disease (PD) is the second most prominent neurodegenerative disease after Alzheimer’s. The onset of the disease is characterized by shaky movements, rigidity of joints, unregulated movements, and even loss of smell. The major cause of this disease is the death of dopaminergic neurons in Substantia Nigra pars compacta (SNc). Dopamine (DA) deficiency due to SNc cell loss manifest as the cardinal PD symptoms that include tremor, rigidity, bradykinesia, and postural imbalance. Epidemiological data indicate that there has been an exponential growth of people suffering from PD over the last few decades. However, the exact cause of this cell death is still not known. Various lines of investigation, experimental and computational, are in progress, and hopefully, we will be able to narrow down the roots of this disease. Understanding the cause and effect relationship between the underlying pathology and symptoms of any neurological disease has fundamental challenges since the roots of the disease are at molecular and cellular levels while the symptoms are seen at the behavioral level. Hence it is important to have a multiscale model that spans molecular mechanisms to behavioral outputs. We are working on developing a patient-specific testbench for Parkinson’s disease where we present a multiscale model of the cortico-basal ganglia (BG) system to simulate arm- reaching movements under normal, parkinsonian, and levodopa medication conditions. At the lowest level, the intracellular molecular pathways of SNc cells are modeled so as to capture dopamine synthesis, uptake, and release. At the next level, the BG circuitry is modeled using rate-coded neurons, which are cast within the reinforcement learning framework with striatum acting as the neural correlate for critic and the direct and indirect pathways facilitating exploitation and exploration, respectively. At the highest level, arm reaching movements are modeled by a two-link arm model driven by a sensory-motor cortical loop. In addition, using same architecture of BG, we are developing an agent model to perform diverse cognitive tasks. We use a rapid assessing cognitive battery to examine diverse cognitive dimensions within the same subject. In this study, we propose a unified computational framework with strong biological underpinnings to explain the observed behavior for functions such as attention, response inhibition, interference processing, and working memory. The final goal is to develop a canonical BG model that can perform various functions of BG and extend the model to pathological conditions in order to come up with disease-modifying therapeutic interventions

Speaker Bio

:

Speaker

:

Giriraj Sahu

Affiliation

:

Ph.D. Assistant Professor, NIPER Ahmedabad

Venue

:

Video Conference

Time

:

10.00AM

Date

:

23 Dec 2021

Abstract

:

NIPER Ahmedabad Ion channels play a vital role in the regulation of neuronal excitability by controlling the generation and transmission of action potentials. A key intrinsic feedback mechanism to control membrane excitability is provided by a calcium-dependent slow afterhyperpolarization (sAHP) in hippocampal pyramidal neurons. The sAHP is important in representing one of the largest inhibitory responses in the brain lasting ~5-10 sec to exert control over the duration, number, and frequency of spike firing. Disruption of the factors contributing to the sAHP in CA1 hippocampal pyramidal cells contributes to aging, epilepsy and neurodegenerative diseases. Yet the molecular mechanisms that underlie the sAHP remained a mystery for over 20 years.

My research work has identified the role of L-type (Cav1.3) calcium channels in activating the calcium-gated potassium channel KCa3.1 to generate the sAHP in CA1 pyramidal neurons (King et al. 2015, Cell Reports; Turner et al., 2016; Sahu et al., 2017, J Neuroscience; 2019, Cell Reports). These studies reflect a combination of patch clamp recordings in an in vitro brain slice preparation, super�resolution fluorescence microscopy, and Fluorescence Resonance Energy Transfer (FRET) to localize protein-protein interactions. Through this, my work defined a new form of calcium-dependent facilitation of Cav1.3 channels and their inclusion in a new triprotein complex of Cav1.3, ryanodine 2 (RyR2) and KCa3.1 potassium channels that work synergistically to activate the sAHP in pyramidal cells. This is unique in that super-resolution stochastic optical reconstruction microscopy (dSTORM) imaging in total internal reflection (TIRF) mode provided a 25-40 nm resolution of the Cav1-RyR2-KCa3.1 complex within 100 nm of the membrane surface. This work highlighted the role of RyRs located in the endoplasmic reticulum (ER) but positioned within 10 nm of the plasma membrane (PM) at specialized ER-PM junctions. dSTORM imaging experiments were complemented with live-cell FRET imaging to reveal the functional assembly of these proteins at ER-PM junctions by the tethering actions of junctophilin 3&4, knockdown of which dissociated the triprotein complex and blocked the sAHP and spike accommodation (Sahu et al., 2019, Cell Reports).

In summary, the conclusions of my work have importance in defining the factors that coordinate excitation and inhibition (E/I) balance by evoking a long duration sAHP that fine-tunes the firing pattern of hippocampal pyramidal neurons. With these developments, my long-term research interests are based on how the function of these novel multiprotein complexes are modulated to alter the network excitability patterns and E/I balance observed in neurobiological disorders like epilepsy and aging. As an outcome of these research, I envision identifying novel drug targets and contribute towards development of advanced therapeutics for complex neurobiological disorders.

Speaker Bio

:

Speaker

:

Dr. Debasish Roy

Affiliation

:

Venue

:

Video Conference

Time

:

09.00AM

Date

:

8 Dec 2021

Abstract

:

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. Swagata Ghatak

Affiliation

:

Scripps Institute.

Venue

:

Video Conference

Time

:

11:30 AM

Date

:

25 Mar 2021

Abstract

:

Excitatory/inhibitory (E/I) balance, defined as the balance between excitation and inhibition of synaptic activity in neuronal network accounts in part for the normal functioning of the brain. In many pathological conditions, this fine balance is perturbed, leading to excessive or diminished excitation relative to inhibition, termed E/I imbalance, reflected in network dysfunction. The mechanisms underlying the E/I imbalance in neurodegenerative and neurodevelopmental disorders are poorly understood leading to a lack of effective therapy. Here, we show that human induced pluripotent stem cell (hiPSC) derived neuronal and cerebral organoid models of Alzheimer’s disease (AD) and MEF2C haploinsufficiency syndrome (MHS), a type of autism spectrum disorder, manifest aberrant electrical activity similar to that observed in patients. Using electrophysiological and cell biological techniques, we found that both active and passive mechanisms acting at the synaptic and neural network-level cause the aberrant hypersynchronous activity in hiPSC derived neuronal models of AD and MHS. We found proteomic differences in AD neurons vs wild-type neurons that were correlated with their electrophysiological differences using a novel single-cell patch proteomics technique. In addition to E/I imbalance, we found miRNA-mediated disruption of neurogenesis and excess gliogenesis in MHS cerebral organoids suggesting a developmental anomaly that may contribute to MHS pathology. Interestingly, NitroSynapsin, an uncompetitive open channel blocker of NMDA receptors, can normalize the imbalance in electrical activity in both AD and MHS by decreasing the excess extrasynaptic current in these neurons and can therefore alleviate some of the pathologies in both hiPSC derived neurons and transgenic mice brain. These findings suggest that therapies aimed at rebalancing the neural network can improve neurological function and provide insight for future drug development.

Speaker Bio

:

Speaker

:

Dr. Ish Venkatesh

Affiliation

:

Research Asst Professor – Marquette University.

Venue

:

Video Conference

Time

:

10:00 AM

Date

:

5 Mar 2021

Abstract

:

Embryonic and peripheral neurons respond to Spinal Cord Injury with activation of transcriptional networks conducive to re-growth, achieving full recovery. In contrast, injured mature CNS neurons fail to re-induce appropriate transcriptional networks, resulting in failed regeneration and permanent damage. We have previously shown that forced re-expression of single transcription factors (TFs) such as KLF6 partially re-activates pro-growth transcriptional networks and promotes axon outgrowth following injury. While this is a promising strategy for therapeutic neural repair, full functional recovery requires an increase in the overall number and regenerative speed of axons. What could be preventing the full efficacy of transcription factor treatments? I have identified three neuron-intrinsic barriers that dampen the effects of transcription factor treatments preventing full recovery. These barriers are (1) Lack of availability of activating TFs (2) Presence of repressive TFs (3) Epigenetic constraints. By reconstructing the transcriptional regulatory landscape in regeneration competent embryonic neurons, I have identified targeted gene candidates to override intrinsic barriers and achieve full recovery in injured mature CNS neurons. These gene candidates will be screened in single-cell assays of gene expression and chromatin accessibility followed by functional testing in in vivo mouse models of Spinal Injuries. Overall, this research is expected to identify novel therapeutic targets to improve regenerative outcomes following Spinal Cord Injury.

Speaker Bio

:

Speaker

:

Dr. Albert Chen

Affiliation

:

Ph.D. Associate Professor,
Scintillon Institute, San Diego, California.

Venue

:

Video Conference

Time

:

10:00 AM

Date

:

25 Feb 2021

Abstract

:

Speaker Bio

:

Speaker

:

Dr. KARA L. MARSHALL

Affiliation

:

Venue

:

Video Conference

Time

:

11:30 AM

Date

:

16 Dec 2020

Abstract

:

PIEZO ion channels detect force in cellular membranes. They are expressed in a wide variety of mammalian tissues, including the vasculature, lymphatic system, and nervous system. We have found that PIEZO2 in sensory neurons is required for the mechanical senses of touch and proprioception, but our understanding of internal organ sensing, interoception, is far behind. I will describe our findings on the role of PIEZO ion channels in the lesser-known interoceptive senses in multiple organ systems.

Speaker Bio

:

Please click and see the attached CV and recent papers.

Speaker

:

Dr. Sergio Neuenschwander

Affiliation

:

Instituto do Cérebro

Venue

:

Video Conference

Time

:

05:00 PM

Date

:

4 Sep 2020

Abstract

:

Gamma responses in the retina are transmitted to the lateral geniculate nucleus and the cortex and are thought to encode stimulus size and continuity (Neuenschwander & Singer, 1996; Ishikane et al., 2005; Roy et al., 2017). In this seminar, I will present a coherence analysis for responses in the retina and LGN of the cat. In a series of experiments, we recorded spiking activity from the LGN of awake animals, subsequently anesthetized with ketamine followed by halothane. Gamma oscillations appeared only when halothane was added to the anesthesia protocol. Notably, in the awake cat, entrainment to the monitor refresh was commonly observed up to 120 Hz. Under halothane, these externally driven rhythms were superseded by gamma responses. These latter findings indicate that endogenously generated oscillations in the early visual system may shorten the representation of fast-changing stimuli. Overall, our results do not support the hypothesis that gamma oscillations in the retina play a role in natural vision. As I will discuss, the synchronization mechanism responsible for response entrainment may also cause fast oscillations in the retinal circuits under anesthesia.

Speaker Bio

:

Speaker

:

Dr. Neeraj Kumar

Affiliation

:

Venue

:

Video Conference

Time

:

04:00 PM

Date

:

6 Aug 2020

Abstract

:

Humans demonstrate a remarkable ability to learn and perform highly skilled actions; movements of dancers, musicians and athletes often leave us in awe. Unsurprisingly, such “motor” learning is known to result in changes in the human motor system. However, recent evidence suggests that learning-related changes also occur in somatosensory areas of the brain. We used non-invasive brain stimulation over the somatosensory cortex to probe the functional contributions of this plasticity. We show that changes in the somatosensory (but not the motor) system are essential for the consolidation of learning; suppressing somatosensory activity prevents a newly formed memory from being consolidated. We also provide evidence that enhancing plasticity in these regions through excitatory brain stimulation increases the retention of learning. Next, I will discuss the contribution of a somatic region (area 46v) in the prefrontal cortex in motor learning. We show that brain stimulation over this area interferes with the transient storage of somatic information that is needed for the repetition of a successful movement. I will end by discussing ongoing work that seeks to exploit these effects and improve motor function in Stroke patients through somatosensory training.

Speaker Bio

:

Dr. Neeraj Kumar completed his PhD in Cognitive Science from IIT Gandhinagar in 2014. His undergraduate training is in Psychology and holds a Master’s degree in Cognitive Science from the University of Allahabad. In 2015, he received an Early Career Fellowship from the Wellcome Trust-DBT India Alliance. During this fellowship, he has worked at IIT Gandhinagar and McGill University. During his stay at McGill, he also collaborated with neurologists to work on a stroke rehabilitation clinical trial. His research is primarily focused on investigating interactions between the motor and sensory systems in the human brain, and draws upon a variety of principles in Psychology and Neuroscience. This work also informs the development of new rehabilitation approaches for patients with movement deficits due to neurological injury.

Speaker

:

Dr. Ashesh Dhawale

Affiliation

:

Center for Brain Science, Harvard University.

Venue

:

Video Conference

Time

:

09:00 AM

Date

:

22 Jul 2020

Abstract

:

Our ability to learn and produce motor skills underlies much of what we do, be it playing instruments or sports, communicating through writing or speech, or simply tying our shoelaces. Yet the neural mechanisms that support these complex behaviors remain unclear. A major reason for this is the lack of experimental tools to follow changes in behavior and associated neural representations over the weeks-to-months long timescales relevant for phenomena such as motor skill learning.

To address this technical gap, I developed new methods to automate the collection and analysis of large, longitudinal datasets of behavior and neural activity in the experimentally tractable rodent model system. These include an experimental platform to track the spiking activity of large ensembles of neurons in behaving animals continuously (24/7) over months-long timescales. I will describe how I used these tools to elucidate the role of the basal ganglia in the execution and maintenance of skilled motor sequences, and to uncover the trial-by-trial algorithms that drive learning in continuous motor spaces. Finally I will outline my proposal to investigate how the brain learns statistical structure in the environment to efficiently solve complex, real-world cognitive tasks.

Speaker Bio

:

Speaker

:

Dr. Santhosh Sethuramanujam

Affiliation

:

University of victoria.

Venue

:

Video Conference

Time

:

10:00 AM

Date

:

1 Jul 2020

Abstract

:

An increasing number of neurons in the brain show the proclivity to release both excitatory and inhibitory neurotransmitters. This is best illustrated by neurons releasing the excitatory neurotransmitter acetylcholine, as these cells invariably also release the inhibitory neurotransmitter, GABA. At first glance, such co-transmission seems an inefficient way to transmit information, as simultaneously exciting and inhibition downstream neurons should cancel the signal. Hence, the mechanisms and functions of co-transmission are poorly understood. In my postdoctoral work, employing a combination of state-of-the-art techniques including 2-photon imaging and optogenetics, I revealed how retinal starburst amacrine cells differentially transmit acetylcholine and GABA—such that it rapidly excites a subset of downstream neurons while simultaneously inhibiting a different population. This differential transmission of acetylcholine and GABA allows the retinal circuitry to compute direction selectivity. Hence, these findings provide one of the first instances explaining the mechanisms employed by neurons in the brain to transmit both excitatory and inhibitory neurotransmitters, and their subsequent role in encoding information

Speaker Bio

:

Speaker

:

Dr. Navneet Vasistha

Affiliation

:

University of Copenhagen.

Venue

:

Video Conference

Time

:

03:00 PM

Date

:

8 Jun 2020

Abstract

:

Mental disorders such as depression, bipolar disorder and schizophrenia are a leading cause of disability worldwide. These have an onset in adolescence or adulthood and result in severe morbidity and decrease the quality of life. Despite the late onset, studies increasingly point towards an impairment in the development of neurons. A precise description of the developmental stages, cell-types and effects is however lacking till date.

Using two distinct mouse models, I highlight a convergence in the developmental etiology of mental disorders. In a model of 15q13.3 microdeletion as well as maternal immune activation (MIA), I show a developmental-stage and subtype dependent effect on interneuron progenitors. This results in a differential impact on specific cortical interneuron subtypes. Specifically, I show a profound reduction in parvalbumin (PV) and somatostatin (SST)-expressing cells in the postnatal cerebral cortex in both models and a lesser impact on caudal ganglionic eminence derived interneurons.

Finally, using publicly available single-cell datasets as well as in-house generated single-nucleus transcriptomics data in 15q13.3 mice, I describe the underlying transcriptomic differences between neuronal subtypes. Understanding the differential vulnerability of interneuron subtypes could provide insights into the variation in phenotypes and severity seen in mental disorders.

Speaker Bio

:

Speaker

:

Dr. Vishnu Sreekumar

Affiliation

:

National Institutes of Health,USA.

Venue

:

Video Conference

Time

:

05:00 PM

Date

:

7 May 2020

Abstract

:

Context is definitional to episodic memory. My research program aims to understand context at different spatiotemporal scales and to test predictions of context-based memory models using both ecologically valid smartphone-based experience sampling data as well as more controlled laboratory-based behavioral and human brain (fMRI, iEEG, and single units) data. I will first describe the spatiotemporal structure of large-scale everyday contexts of people’s lives and demonstrate that this measured structure corresponds to brain activity patterns during reminiscence. I’m particularly interested in understanding temporal context, a gradually changing state to which events are bound as we experience them, and will describe how temporal context is represented in the brain at different spatial and temporal scales. I will provide direct neural evidence using intracranial EEG for model predictions based on the assumption that associated temporal context is retrieved when we remember events. Finally, I will describe the temporal context as coded by single units in the human brain. I will discuss future avenues combining ecological validity and experimental control to further investigate the role of context in memory.

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

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13 Jun 2018

Abstract

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Speaker Bio

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Speaker

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Dr. Vivek Swarup

Affiliation

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

Venue

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CNS Seminar Hall, Ground Floor

Time

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4:00 PM

Date

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25 Apr 2018

Abstract

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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

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