Events

lecture

Tuesday, November 25, 2025
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

Computational trade-offs as a core principle of brain function

Dr. Yuval Hart

lecture

Tuesday, May 27, 2025
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

Unlocking the Night: Novel Approaches Advancing the Neuroscience of Sleep and Cognition

Prof. Yuval Nir

In this talk, I will present recent studies in our lab, where new tools are pushing the boundaries of sleep research.In a first line of studies, we are investigating how sleep promotes memory consolidation in humans. To this end, we developed a novel ecological paradigm to study episodic memory without report; upon repeated viewing of special movies ,eye gaze patterns can quantify memory for specific events. Next, we show that deep brain closed-loop intracranial electrical stimulation during human sleep enhances hippocampus-cortex synchrony and memory performance. Finally, we examine how sleep and memory are disrupted in amnestic mild cognitive impairment (aMCI) representing early Alzheimer’s disease (AD). To this end, we developed a novel
machine learning-based method to non-invasively detect interictal spikes occurring in the medial temporal lobe during sleep. This approach can help identify disruptions in hippocampus-cortex synchrony and memory consolidation during sleep.

In the second line of studies, we investigate how reduced locus coeruleus-noradrenaline (LC-NE) activity during sleep mediates sensory disconnection. In rodents, the level of ongoing tonic LC activity during sleep anticipates sound-evoked awakenings, while minimal optogenetic LC activation or silencing increases and decreases such awakenings, respectively. Projection-specific investigation in mice indicates that an early surge of brainstem NE is particularly important for mediating sensory-evoked awakenings. These findings may shift how we view arousal- promoting neuromodulation; rather than acting in a diffuse hormonal-like manner, the LC-NE system may in fact operate through specific projection pathways, in a circuit-like manner. Finally, I will describe a novel method for monitoring gaze direction and pupil size through closed eyes in humans via short-wave infrared (SWIR) imaging in combination with video analysis algorithms. This technology has potential to enable touchless and continuous monitoring of depth of anesthesia, pain, and detection of intraoperative awareness.

lecture

Tuesday, May 20, 2025
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

Trauma Under Psychedelics: How trauma during altered states of consciousness impacts cognitive, physiological, neural, and clinical outcomes

Prof. Roy Salomon

lecture

Tuesday, April 22, 2025
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

Cognitive processing in the cerebellum

Prof. Michael E. Goldberg

lecture

Tuesday, March 11, 2025
12:30 - 14:00

Gerhard M.J. Schmidt Lecture Hall

What is special about activity in the basal ganglia?

Prof. Mati Joshua

lecture

Tuesday, February 25, 2025
12:30 - 14:00

Gerhard M.J. Schmidt Lecture Hall

Network models for memory storage with biologically constrained synapses: implications for representational drift.

Dr. Alex Roxin

lecture

Tuesday, February 18, 2025
12:30 - 14:00

Gerhard M.J. Schmidt Lecture Hall

Cell type dependent computations and learning in primary motor cortex

Prof. Jackie Schiller

lecture

Tuesday, February 11, 2025
12:30 - 14:00

Information processing in the vomeronasal system

Prof. Yoram Ben-Shaul

lecture

Wednesday, January 22, 2025
11:00 - 13:00

Deciphering the role of the DCC/UNC-40 receptor in dopaminergic neurons during health and disease

Sapir Sela

TheUNC-40 receptor, a homolog of the human DCC receptor, is critical for neuronal development and maintenance, with its dysregulation implicated in neurodegenerative diseases such as Parkinson’s disease. This study investigates the role of UNC-40 in dopaminergic neuron health and degeneration using Caenorhabditis elegans as a model system. Loss-of-function mutations in UNC-40 conferred resistance to 6-hydroxydopamine (6-OHDA)-induced DA neuron degeneration, while stabilization of UNC-40 via mutation in the CPD regulatory site led to spontaneous, selective DA neurodegeneration independent of toxins. Mechanistic analyses revealed that UNC-40 stabilization triggers parthanatos, a caspase-independent cell death pathway driven by mitochondrial oxidative stress. Pharmacological inhibition of PARP-1 and treatment with mitochondrial antioxidants significantly rescued DA neurons from degeneration.suggesting UNC-40 stabilization causes mitochondrial oxidative stress. Remarkably, UNC-40-induced degeneration was sexually dimorphic, affecting hermaphrodites but not males. Transcriptomic analyses revealed significant gene expression changes in hermaphrodites carrying stabilized UNC40, while males exhibited minimal changes, suggesting intrinsic protective mechanisms. UNC-6, a ligand for UNC-40, was identified as a critical external factor modulating this dimorphism; its absence in hermaphrodites rendered them vulnerable, while its presence in males made them unaffected by the stabilization of the receptor. Behavioral assays revealed functional impairments in hermaphrodites with stabilized UNC-40, linked to altered synaptic activity and excitotoxicity. These findings establish UNC-40 as a key regulator of DA neuron health, highlight its role in oxidative stress and synaptic maintenance, and underscore sexually dimorphic vulnerability to neurodegeneration. The parallels between UNC-40 in C. elegans and DCC in humans suggest conserved mechanisms underlying neurodegeneration and point to potential therapeutic targets for diseases like PD.

lecture

Tuesday, January 21, 2025
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

The Evolution and Plasticity of the CONNECTOME

Prof. Yaniv Assaf

lecture

Monday, January 20, 2025
11:00 - 12:15

Neuromodulation of experience-dependent sexually dimorphic learning

Sonu Kurien Dr. Meital Oren Lab

lecture

Wednesday, January 8, 2025
11:15 - 12:45

Prof. Oded Rechavi

lecture

Thursday, December 5, 2024
12:30 - 13:30

Neuroprotective and Anticonvulsant Effects of Cannabinoids with Neurotrauma

Prof.Linda Friedman

Traumatic brain (TBI) injuries result in profound local hypoperfusion, ischemia, chronic inflammation and refractory seizures(post-traumatic epilepsy (PTE)), and restrict drug delivery to the site of impact so that peripheral treatment alone would have limited access to the site of injury during the most critical phases of neurotrauma. Cannabidiol (CBD), the major non-psychotropic cannabinoid, has anti-convulsant, anti-inflammatory, anti-nociceptive, antioxidant, and immuno-suppressive properties not fully understood. In pre-juvenile rats, microinjection of CBD attenuated kainate(KA)-induced seizures to a greater extent than intraperitoneal injection, indicating that local drug administration was more effective. In adult rats after experimental TBI, our modified CBD-infused implant applied extradural with oil injection supplementation restored vestibulomotorand cognitive functions compared to systemic treatment alone. We questioned whether the CBD or the low concentrations of THC in the extract was responsible for behavioral and cellular recovery.We hypothesized that an optimal ratio of cannabidiol (CBD) to tetrahydrocannabinol (THC) is required to protect against neuropathological consequences following TBI greater than either substance alone. Varied CBD:THC extract concentrations were compared with hempCBD lacking THC (CBD0). Neurons, glia, and parvalbumin interneurons (PV-INs) were evaluated. Weight loss was observed following high doses of THC dominant cannabis, THC100:1. Neuroscoresand vestibulomotorperformance were restored more with CBD:THC300:1-10:1. However, THC dominant treatments resulted in early onset to spontaneous seizures post-TBI. In a non-reward T-maze, the CBD10:1group had the highest alternation rates; TBI + vehicle, CBD0, CBD1:1, and THC100:1treatment groups had the lowest. The novel object recognition memory task showed CBD300:1treated animals had the best performance, while TBI or THC100:1treated groups had the worst. The forced swim test (FST) showed immobility time was highest after TBI and lowest after THC100:1treatment. The elevated plus maze (EPM) revealed the CBD0group spent the most time in closed arms. Both tests indicate that reduced anxiety was THC dependent. All combinations resulted in reduced injury but CBD10:1and THC20:1gave the most protection and THC100:1the least. Reduced anxiety level was THC dependent but higher doses were pro-convulsant cautioning THC dosing. Reduced GFAP labeling was highest with CBD dominant cannabis supporting its neuroprotective role against inflammation. Rescue of diminished bilateral PV-INs was observed within the hippocampus and medial prefrontal cortex (mPFC) with CBD dominant treatment (CBD300, CBD0) supporting their anticonvulsant effect. Loss of PV-INs with THC dominant treatment supports their proconvulsant effect. Thus, CBD and THC have different beneficial therapeutic effects indicating an optimal concentration ratio is critical for optimal neuropathological therapeutics.

Light refreshments before the seminar

lecture

Tuesday, December 3, 2024
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

The Evolution of 7T (and Beyond) MRI in Basic Research and Clinical Practice

lecture

Monday, October 14, 2024
15:00 - 17:00

Gerhard M.J. Schmidt Lecture Hall

The role of neurons in the direction-selective retinal circuit in visual processing in the retina and in the visual thalamus

Alina Heukamp-Prof. Michal Rivlin Lab

lecture

Thursday, July 11, 2024
11:00 - 12:00

Gerhard M.J. Schmidt Lecture Hall

Designing Language Models to Think Like Humans

Dr. Chen Shani

Prof. Pablo Blinder

lecture

Tuesday, May 28, 2024
12:30 - 13:15

Gerhard M.J. Schmidt Lecture Hall

Vasosdynamics of cortical arterioles and what it informs us about neuronal activity

lecture

Tuesday, May 7, 2024
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

My lab’s focus in recent years has been split between development of ultra-high resolution fMRI at high field and the exploration of more sensitive yet robust methods to find all the salient transients and trends in the signal. High field, high resolution fMRI relies heavily on the acquisition technology and the functional contrast used as well as unique processing approaches that segment, as well as possible, cortical layers for analysis. Our fMRI time series analysis research relies on creative paradigm design in conjunction with tailored processing methods that strike a balance between casting a wide net for potentially informative signals and applying just enough modeling to make sense of the data. Our goal is to use fMRI to see neuronal activity and capture neural correlates of behavior that have previously been elusive to more standard approaches. Specifically, for our high resolution fMRI work, I will describe experiments demonstrating layer-specific activity in motor, somatosensory, and visual cortex that changes with tasks that modulate the hypothesized input and output cortical communication. In our lab, we perform layer fMRI using a functional contrast called VASO (vascular space occupancy) that is sensitive to blood volume changes in micro vessels - having more specificity than BOLD with only a small tradeoff in sensitivity. Layer fMRI has the potential to provide cortical hierarchy information and communication directionality based on the understanding that feedforward connections terminate predominantly in middle layers and feedback connections terminate in predominantly upper and lower layers. Hence by determining activation location across cortical depth, one can infer whether the activation is feedforward or feedback. I will also demonstrate how the use of resting state connectivity in conjunction with layer fMRI is able to discern such cortical hierarchy in visual areas. Lastly, I will also show examples of applications of layer fMRI in frontal cortex during a working memory task. In addition, I will show our high resolution fMRI work that has allowed us to discern a new digit organizational pattern in motor cortex. For our time series work, I will show our recent results in using connectivity-based decoding for identifying, in an unsupervised manner, tasks being performed. In addition, I will show an application of naturalistic stimuli and inter subject correlation to characterize personality trait and language skills of individuals. Lastly, changes arousal state during scanning has been viewed as both a confound and opportunity. I demonstrate our effort to further characterize the temporal and spatial signatures of arousal state changes in fMRI time series.

lecture

Tuesday, January 3, 2023
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

Latent cause inference in learning and decision making

Prof. Yael Niv

lecture

Monday, January 2, 2023
11:15 - 12:15

Arthur and Rochelle Belfer Building for Biomedical Research

Renewal and plasticity in oral and gastrointestinal epithelia

Prof. Ophir Klein

lecture

Tuesday, December 13, 2022
12:30

Gerhard M.J. Schmidt Lecture Hall

How movement regulates defensive behaviours in a social context

Prof. Marta Moita

Our work concerns the general problem of adaptive behavior in response to predatory threats, and of the neural mechanisms underlying a choice between strategies. Interacting predators and prey tightly regulate their motion, timing with precision when to hold, attack or escape. Motion cues are thus paramount in these interactions. Speed and (un)predictability have shaped the evolution of sensory and motor systems, the elucidation of which a great deal of research has been devoted. Much less attention has been paid to the role of motion as a social cue of threat or safety. We and others have found that prey animals use the movement of their neighbors to regulate their defensive responses. We have studied social regulation of freezing in rodents and found that rats use cessation of movement evoked sound, resulting from freezing, as a cue of danger. In addition, auto-conditioning, whereby rats learn the association between shock and their own freezing, during prior experience with shock, facilitates the use of freezing by others as an alarm cue. To further explore the social regulation of defensive responses we resorted to the use fruit flies as it easily allows testing of groups of varying sizes, the collection of large data sets and genetic access to individual neuronal types. We established that fruit flies in response to visual looming stimuli, simulating a large object on collision course, make rapid freeze/flee choices accompanied by lasting changes in the fly’s internal state, reflected in altered cardiac activity. Freezing in flies is also strongly modulated by the movement of surrounding neighbours. In contrast with rodents that use auditory cues, female flies use visual motion processed by visual projection neurons. Finally, I will discuss more preliminary findings suggesting that there are multiple states of freezing as measured by muscle activity in the fly legs. Having established the fly as a model to study freezing/fleeing decisions, we are in a great position to perform large scale integrative studies on the organization of defensive behaviours. Short Bio Marta Moita received her BSc degree in Biology at the University of Lisbon, in 1995. As part of Gulbenkian’s PhD programme in Biology and Medicine she developed her thesis work, on the encoding by place cells of threat conditioning under the supervision of Prof. Joseph Ledoux, at the New York University (1997-2002). In 2002, Marta Moita worked as a postdoctoral fellow in Dr. Tony Zador’s laboratory, at the Cold Spring Harbor Laboratory, to study the role of auditory cortex in sound discrimination. In 2004, she became a principal investigator, leading the Behavioral Neuroscience lab, at the Instituto Gulbenkian de Ciência. In 2008 her group joined the starting Champalimaud Neuroscience program. In 2018 and 2019 Marta Moita served as Deputy Director of Champalimaud Research. Her lab is primarily interested in understanding the mechanisms of behavior. To this end, the lab has focused on behaviors that are crucial for survival and present in a wide range of species, namely defensive behaviors triggered by external threats. Using a combination of state-of-the-art tools in Neuroscience (initially using rats and currently using fruit flies) and detailed quantitative descriptions of behavior, her lab aims to understand how contextual cues guide the selection between different defensive strategies and how the chosen defensive behavior and accompanying physiological responses are instantiated.

lecture

Wednesday, November 30, 2022
14:00 - 15:00

Deciphering non-neuronal cells contribution to Alzheimer’s disease pathology using high throughput transcriptomic and proteomic methods

Dept of Brain Sciences,Dr. Michal Schwartz,Sedi Medina (PhD Thesis Defense Seminar) on Zoom

Prof. Shabtai Barash

lecture

Thursday, February 10, 2022
09:00 - 10:00

Effects of physical exercise and adult neurogenesis on hippocampal neural codes

Yoav Rechavi - PhD Thesis Defense on Zoom

lecture

Tuesday, February 1, 2022
12:30

Theory of neural perturbome

Prof. Claudia Clopath

lecture

Tuesday, January 25, 2022
12:30

Gerhard M.J. Schmidt Lecture Hall

To be announced

Alex Borst

lecture

Tuesday, January 25, 2022
10:00 - 11:15

Prof. Naoshige Uchida

lecture

Monday, January 10, 2022
14:00 - 16:00

Circuits for decisions, attention and working memory in the primate visual system

Dr. Leor Katz

lecture

Wednesday, January 5, 2022
10:00 - 11:00

Prof. Inna Slutsky

lecture

Tuesday, November 2, 2021
12:30 - 13:30

Brain-wide networks underlying behavior - Insights from functional ultrasound imaging

lecture

Tuesday, October 26, 2021
12:30 - 13:30

Gerhard M.J. Schmidt Lecture Hall

Nonoscillatory coding and multiscale representation of very large environments in the bat hippocampus by Tamir Eliav and There is Chemistry in Social Chemistry by Inbal Ravreby

Dept of Brain Sciences,Dr. Tamir Eliav,Prof. Nachum Ulanovsky,Prof. Noam Sobel

Nonoscillatory coding and multiscale representation of very large environments in the bat hippocampus Abstract: The hippocampus plays a key role in memory and navigation, and forms a cognitive map of the world: hippocampal ‘place cells’ encode the animal’s location by activating whenever the animal passes a particular region in the environment (the neuron’s ‘place field’). Over the last 50 years of hippocampal research, almost all studies have focused on rodents as animal models, using small laboratory experimental setups. In my research, I explored hippocampal representations in a naturalistic settings, in a unique animal model – the bat. My talk will outline two main stories: (i) In rodents, hippocampal activity exhibits ‘theta oscillations’. These oscillations were proposed to support multiple functions, including memory and sequence formation. However, absence of clear theta in bats and humans has questioned these proposals. Surprisingly, we found that in bats hippocampal neurons exhibited nonoscillatory phase-coding. This highlights the importance of phase-coding, but not oscillations per se, for hippocampal function across species – including humans. (ii) Real-world navigation requires spatial representation of very large environments. To investigate this, we wirelessly recorded from hippocampal dorsal CA1 neurons of bats flying in a long tunnel (200 meters). Place cells displayed a multifield multiscale code: Individual neurons exhibited multiple place fields of diverse sizes, ranging from 0.6 to 32 meters, and the fields of the same neuron differed up to 20-fold in size. Theoretical analysis showed that the multiscale code allows representing large environments with much better accuracy than other codes. Thus, by increasing the spatial scale, we uncovered a neural code that is radically different from classical spatial codes. Together, these results highlight the power of the comparative approach, and demonstrate that studying the brain under naturalistic settings and behavior enables discovering new unknown aspects of the neural code. There is Chemistry in Social Chemistry Abstract: Non-human terrestrial mammals constantly sniff themselves and each-other, and based on this decide who is friend or foe. Humans also constantly sniff themselves and each-other, but the functional significance of this behavior is unknown. Given that humans seek friends who are similar to themselves, we hypothesized that humans may be smelling themselves and others to subconsciously estimate body-odor similarity, and that this may then promote friendship. To test this hypothesis, we recruited non-romantic same-sex friend dyads who had initially bonded instantaneously, or so called click-friends, and harvested their body-odor. In a series of experiments, we then found that objective ratings obtained with an electronic nose, and subjective ratings obtained from independent human smellers, converged to suggest that click-friends smell more similar to each other than random dyads. To then estimate whether this similarity was merely a consequence of friendship, or a driving force of friendship, we recruited complete strangers, smelled them with an electronic nose, and engaged them in non-verbal same-sex dyadic interactions. Remarkably, we observed that dyads who smelled more similar had better dyadic interactions. In other words, we could predict social bonding with an electronic nose. This result implies that body-odor similarity is a causal factor in social interaction, or in other words, there is indeed chemistry in social chemistry.

lecture

Tuesday, October 19, 2021
10:00 - 11:00

Social Behavior in a Social Context: Lessons from Studying Genetic and Neuronal Manipulations affecting Social Behavior in a Complex Environment

Noa Eren (PhD Thesis Defense)

As methods for highly specific and precise manipulations of genetics and neuronal activity become the standard in neuroscience, there is growing demand for behavioral paradigms to evolve as well, beyond the simplified and reductive tests which are commonly used. This is especially evident in social behavior, where standard testing paradigms are typically short, involve only a pair of animals, and take place in stimulus-poor environments. Here, we present a series of studies using the Social Box, an experimental setup developed in our lab to automatically track groups of mice living in an enriched environment over days, and extract dozens of behavioral readouts at the individual, dyadic, and group level. We manipulated neuronal populations expressing the socially-relevant neuropeptides oxytocin (OXT) and urocortin3 (UCN3), and utilized genetic mouse models of human disorders affecting sociability – autism spectrum disorder (ASD) and Williams-Beuren Syndrome (WBS) – to demonstrate the importance of the social context in studying mouse behavior. Repeated optogenetic activation of Oxt+ cells recapitulated the known effect of reducing aggressive behavior in the classical resident-intruder paradigm, but in a group of conspecifics it led to an increase in such behaviors on the second day of activation. In parallel, chemogenetic activation of Oxt+ or Ucn3+ cells, separately or together, increased aggressive behavior in the context of a territorial conflict. Finally, behavior of ASD-like mice was mediated by the group composition, such that single-genotype groups showed greater genotype separation in multi-behavioral space than mixed-genotype groups. These findings emphasize the importance of considering contextual and environmental factors when designing and interpreting behavioral studies, which could affect the translatability of findings from mouse to human. Zoom link to join: https://weizmann.zoom.us/j/94822556146?pwd=VnY2eDVGeWdSNmFCVC9zZDVrWUtvUT09 Meeting ID: 948 2255 6146 Password: 884034

Raz Dvir-Szternfeld (PhD Thesis Defense)

Alzheimer’s disease (AD) is an age-related neurodegenerative disorder, which is the most common cause of dementia. Among the key hallmarks of AD are neurofibrillary tangles, abnormal amyloid beta (A) aggregation, neuroinflammation and neuronal loss; altogether manifested in progressive cognitive decline. Numerous attempts were made to arrest or slow disease progression by directly targeting these factors, with a limited successes in having a meaningful effect on cognition. In the recent years, the focus of AD research has been extended towards exploring the local and systemic immune response. Yet, the role of the two main myeloid populations, the central nerve system (CNS) resident immune cells, microglia and blood-borne monocyte-derived macrophages (MDM) remain unclear. In my PhD, together with members of the teams, using behavioral, immunological, biochemical and single-cell resolution molecular techniques, we deciphered the distinct role of microglia and MDM in transgenic mouse models of AD pathology. Using single cell RNA sequencing (scRNA-seq) in 5xFAD amyloidosis mouse model, we have identified a new state of microglia, which we named disease associated microglia (DAM) that were found in close proximity to A plaques. The full activation of these cells was found to be dependent on Triggering receptor expressed on myeloid cells 2 (TREM2), a well-known risk factor in late onset AD. To get an insight to the role of MDM relative to microglia, we used an experimental paradigm of boosting the systemic immunity by modestly blocking the inhibitory immune checkpoint pathway, PD-1/PD-L1, which was previously shown to be beneficial in ameliorating AD in 5xFAD mice, via facilitating homing of MDM to the brain. We found that the same treatment is efficient also in mouse model of tauopathy and that the MDM homing to the brain following the treatment expressed a unique set of scavenger molecules, including macrophage scavenger receptor 1 (MSR1). We found that MDM expressing MSR1 are essential for the disease modification. Using the same immune-modulatory treatment in a mouse model deficient in TREM2 (Trem2-/-5xFAD) and thus in DAM, allowed us to distinguish between the contribution to the disease modification of MDM and DAM. We found, that MDM display a Trem2-independent role in the cognitive improvement. In both Trem2-/-5xFAD and Trem2+/+5xFAD mice the treatment effect on behavior was accompanied by a reduction in the levels of hippocampal water-soluble Aβ1-42, a fraction of A that contains toxic oligomers. In Trem2+/+5xFAD mice, the same treatment seemed to activate additional Trem2-dependent mechanism, that could involve facilitation of removal of Aβ plaques by DAM or by other TREM2-expressing microglia. Collectively, our finding demonstrates the distinct role of activated microglia and MDM in therapeutic mechanism of AD pathology. They also support the approach of empowering the immune system to facilitate MDM mobilization as a common mechanism for treating AD, regardless of primary disease etiology and TREM2 genetic polymorphism.

lecture

Wednesday, August 4, 2021
10:30

Gerhard M.J. Schmidt Lecture Hall

Prof. Galia Avidan

On places and borders in the brain

Prof. Dori Derdikman

lecture

Tuesday, January 26, 2021
12:30 - 13:30

Layers of primary visual cortex as a window into internal models about predicted and simulated environments

Prof. Lars Muckli

lecture

Tuesday, January 19, 2021
12:30

Prof. Shlomo Wagner

lecture

Thursday, December 24, 2020
15:00 - 16:00

Chemosignals are a form of human social communication

Eva Mishor (PhD Thesis Defense)

lecture

Wednesday, December 23, 2020
10:00 - 11:00

Raviv Pryluk (PhD Thesis Defense)

Environmental affordances and the neural representation of complex space

Prof. Kate Jeffery

lecture

Monday, June 17, 2019
13:30

Arthur and Rochelle Belfer Building for Biomedical Research

Externally and internally induced arousal states modify spontaneous and evoked synaptic activities in the mouse somatosensory cortex

Akiva Rapaport (PhD Thesis Defense)

Behavioral states, such as arousal and attention are defined by a set of psychological and physiological variables. They have profound effects on sensation, perception, learning, and cognition. In the brain, global states are characterized by distinct cortical and hippocampal EEG patterns. These changes that are clearly observed in the local field potential (LFP) are also evident in network and cellular dynamics. At the population level, the more active states are manifested as asynchronous neuronal firing between neighboring cells. At the cellular level, the membrane potential during active states is characterized by a continuous depolarized state, high synaptic ac! tivity, reduced variance and reduced membrane potential correlations between cells. In recent years it has been demonstrated in rodents that pupil size is a robust indicator of a range of neural activity from neuromodulator release to cortical neuronal membrane potential. There has been some debate in the field regarding to what extent the effects of locomotion on cortical dynamics are due to arousal and what can be attributed to locomotion. Furthermore, in some studies cortical dynamics were evaluated while the animals transitioned spontaneously between states and in others, states of arousal were externally induced. Additionally, different effects have been reported in the auditory and visual cortex. Therefore, we wanted to more finely differentiate between different states and evaluate the effect of state on the somatosensory cortex. To accomplish this we conducted intracellular recordings in the barrel cortex as well as extracellular LFP recordings in Layer IV of the barrel cortex in awake head fixed mice. We monitored pupil size as an indicator for state of arousal as well as tracking locomotion. We found that there is a significant correlation between membrane potential of cells in barrel cortex and pupil size. Neurons were significantly more depolarized as the animal was in a greater state of arousal. This change was not affected by the mode of inducement of arousal, be it a spontaneous transition into a state of arousal or one externally induced. However, the effect was abolished by the occurrence of locomotion. We also found that responses to sensory stimuli are increased during a state of arousal but not in a state of hyper-arousal. Inducing the state externally minimized this effect and if the animal is locomoting then the increase in sensory responses is abolished. We further found that when the animal is in a greater state of arousal there is less synchronization as indicated by the decrease in correlation between membrane potential and LFP. Even more startlingly, we found that the polarity of the cross-correlation was reversed during hyperarousal. This would strongly suggest a reorganization of the laminar network across different states.

lecture

Sunday, June 16, 2019
11:00

Camelia Botnar Building

A Comprehensive Mechanistic Biological Theory of Brain Function

Prof. Ari Rappoport

conference

Tuesday, June 11, 2019
08:30 - 18:00

The David Lopatie Conference Centre

Prof. Daniel Palanker

Dr. Daniel Gitler

lecture

Thursday, October 18, 2018
12:30

Gerhard M.J. Schmidt Lecture Hall

Information processing at hippocampal synapses

,Prof. J. Simon Wiegert

lecture

Sunday, October 14, 2018
10:30

Gerhard M.J. Schmidt Lecture Hall

Serotonin and Autism Therapeutics: Insights from Human Mutations and Mouse Models

Dr. Randy Blakely

lecture

Sunday, October 7, 2018
12:30 - 13:30

Nella and Leon Benoziyo Building for Brain Research

"What is it like to be a bat?" - A pathway to the answer from the Integrated Information Theory

Dr. Naotsugu Tsuchiya

What does it feel like to be a bat? Is conscious experience of echolocation closer to that of vision or audition? Or, echolocation is non-conscious processing and it doesn't feel anything? This famous question of bats' experience, posed by a philosopher Thomas Nagel in 1974, clarifies the difficult nature of the mind-body problem. Why a particular sense, such as vision, has to feel like vision, but not like audition, is puzzling. This is especially so given that any conscious experience is supported by neuronal activity. Activity of a single neuron appears fairly uniform across modalities, and even similar to those for non-conscious processing. Without any explanation on why a particular sense has to feel as the way it does, researchers even cannot approach the question of the bats' experience. Is there any theory that gives us a hope for such explanation? Currently, probably none, except for one. Integrated Information Theory (IIT), proposed by Tononi in 2004 has a potential to offer a plausible explanation. IIT essentially claims that any system that is composed of causally interacting mechanisms can have conscious experience. And precisely how the system feels like is determined by the way the mechanisms influence each other in a holistic way. In this talk, I will give a brief explanation of the essence of IIT and provide initial empirical partial tests of the theory, proposing a potential scientific pathway to approach bats' conscious experience. If IIT, or its improved or related versions, is validated enough, it will gain credibility to accept its prediction on rough nature of bats' experience. If we can gain a sophisticated insight as to whether bats' experience is closer to vision or audition, it is already a tremendously big step in consciousness science, which is just a first yet critical one, possibly a similar level of the breakthrough in cosmology in precisely estimating the age of the universe. References: 0) talk slide: https://www.slideshare.net/NaoNaotsuguTsuchiya/17-june-20-empirical-test-of-iit-dresden 1) Andrew M. Haun, Masafumi Oizumi, Christopher K. Kovach, Hiroto Kawasaki, Hiroyuki Oya, Matthew A. Howard, Ralph Adolphs, Naotsugu Tsuchiya, (2017, accepted) “Conscious perception as integrated information patterns in human electrocorticography” eNeuro link 2) Tsuchiya “"What is it like to be a bat?" - a pathway to the answer from the Integrated Information Theory ” Philosophy Compass (2017) link 3) Oizumi M, Tsuchiya N, Amari S, “Unified framework for quantifying causality and integrated information in a dynamical system” (2016) PNAS link

lecture

Thursday, August 30, 2018
12:30

Gerhard M.J. Schmidt Lecture Hall

Dynamics of social representations in the prefrontal cortex and their alterations in mouse models of autism

Dana Rubi Levy (PhD Thesis Defense)

lecture

Wednesday, August 29, 2018
10:30

Gerhard M.J. Schmidt Lecture Hall

Learning probabilistic representations in randomly connected neural circuits

Ori Maoz (PhD Thesis Defense)

lecture

Monday, August 13, 2018
10:00 - 11:15

Gerhard M.J. Schmidt Lecture Hall

Catecholamines in the hippocampal formation

Sima Verbitsky (PhD Thesis Defense)

Monoaminergic (noradrenergic, dopaminergic and serotonergic) modulation of hippocampal activity is assumed to play a major role in neuronal plasticity, learning and memory. Understanding the locus of action of these neuromodulators at the cellular level will expand our knowledge of their nature and allow us to identify issues related to their dysfunction. In the present work I study the effects of norepinephrine (NE) and dopamine (DA) on spontaneous and evoked activity in patch-clamped neurons of hippocampal slices. Both DA and NE induced a significant decrease in the amplitude of the evoked PSCs recorded from CA1 pyramidal neurons in response to stimulation of the Schaffer collaterals, accompanied by a small decrease in the cell input resistance, and a small hyperpolarization. While decreasing the evoked PSCs, NE promoted an overall increase in spontaneous synaptic activity. Pharmacological assessment of these results indicated an α1 adrenergic receptor involvement in both the decrease of the amplitude of evoked PSCs as well as the increase in spontaneous activity. Surprisingly, the effect of NE on evoked PSCs was partially antagonized by D1 dopaminergic receptor antagonist SCH23390, which suggests that NE activates dopamine receptors. The effect of DA on evoked PSCs was blocked by α1 adrenergic receptor antagonist prazosin, which suggests that DA, in turn, is activating adrenergic receptors. Noradrenergic system is highly affected by stress; in particular, the differences between NE effects in dorsal and ventral hippocampus (DH and VH, respectively) have been shown to change in stressed animals. In this work I used two types of stress protocols – Prenatal Stress (PS) and Acute Stress (AS) – to study the effect of stress on monoamine responses in slices of DH and VH. In non-stressed rats, NE effect on the evoked PSCs is larger in DH than in VH. PS and AS rats increased NE effect in VH, thus abolishing the difference between DH and VH. Pharmacological data suggests that these differences result from differential efficiencies of α1 and D1 receptors between DH and VH of both control and PS rats. Acute stress reversed the difference between PS and control rats; in the AS slices the PSC reduction was significantly different between DH and VH of PS rats, and not in control rats. I conclude that stress increases the NE modulation in VH, but not in DH, thus increasing the role of emotional processing associated with the VH.

lecture

Sunday, August 12, 2018
15:00

Nella and Leon Benoziyo Building for Brain Research

Regulation of the blood-cerebrospinal fluid barrier as a gateway for leukocyte trafficking in physiology and pathology

Alexander Kertser (PhD Thesis Defense)

lecture

Wednesday, August 1, 2018
14:00

Nella and Leon Benoziyo Building for Brain Research

The role of TrpC2 channel in mediating social behavior of male mice within a group

Yefim Pen (PhD Thesis Defense)

lecture

Thursday, July 26, 2018
11:00

Gerhard M.J. Schmidt Lecture Hall

Prof. Alexey Semyanov

Brain is often viewed as large neuronal connectome where the information is encoded in the patterns of action potentials and stored in the changes of synaptic strength or appearance of new wiring routes. However, recent studies have demonstrated that astrocytes also possess complex patterns of calcium signals influenced by neuronal activity. Astrocytic calcium signals regulate various functions of these cells including release of gliotransmitters and morphological changes in the astrocytic processes (Tanaka et al., 2013). It has been tempting to suggest that information in astrocytes is encoded in the frequency of calcium events, similar to patters of neuronal action potentials. Synaptically released neurotransmitters thought to trigger new calcium events in perisynaptic astrocytic processes (PAPs) though activation of metabotropic glutamate receptors (mGluRs). In contrast, our recent findings suggest that PAPs are devoid of calcium stores that are required for mGluR-mediated calcium signaling (Patrushev et al., 2013). This makes unlikely any significant role of mGluRs in triggering calcium events in PAPs. Instead, we show that activation of ‘extrasynaptic’ astrocytic mGluRs increases proportion of spatially extended calcium events in the power-law based distribution of calcium event sizes (Wu et al., 2014). This effect takes place without any significant increase in the frequency of calcium events. These findings suggest that astrocytic response to surrounding neuronal activity is rather encoded in spatial characteristics of their calcium events and fundamentally different from temporal information coding in neurons (e.g. coincidence detection, action potentials sequences etc). Nevertheless, we cannot exclude local ionic changes in PAPs in response to synaptic activity. For example, potassium ions accumulate in the synaptic cleft of glutamatergic synapses during repetitive activity. We have demonstrated that the bulk of these ions is contributed by potassium efflux through postsynaptic NMDA receptors (Shih et al., 2013). Potassium mediated depolarization of presynaptic terminal increases glutamate release probability. Now we have found that accumulation of intracleft potassium during repetitive synaptic activity could also inhibit astrocytic glutamate uptake by depolarizing PAPs. This extends glutamate dwell-time in the synaptic cleft and boosts glutamate spillover effects.

lecture

Monday, May 28, 2018
12:30

Gerhard M.J. Schmidt Lecture Hall

From dragons’ sleep to sliders’ sight: reexamination of reptilian model systems

Dr. Mark Shein-Idelson

lecture

Tuesday, May 15, 2018
12:30

Gerhard M.J. Schmidt Lecture Hall

Synaptic dynamics in mouse visual cortex

Dr. Tara Keck

lecture

Sunday, May 13, 2018
10:00

Nella and Leon Benoziyo Building for Brain Research

In vivo identification of brain structures functionally involved in spatial learning and strategy switch

Dr. Suellen DeAlmeida-Correa

Prof. Elly Nedivi

conference

Monday, March 26, 2018
08:00

Dolfi and Lola Ebner Auditorium

Prof. Rita Z. Goldstein, PhD

Drug addiction is a chronically relapsing disorder characterized by compulsive drug use despite catastrophic personal consequences (e.g., loss of family, job) and even when the substance is no longer perceived as pleasurable. In this talk, I will present results of human neuroimaging studies, utilizing a multimodal approach (neuropsychology, functional magnetic resonance imaging, event-related potentials recordings), to explore the neurobiology underlying the core psychological impairments in drug addiction (impulsivity, drive/motivation, insight/awareness) as associated with its clinical symptomatology (intoxication, craving, bingeing, withdrawal). The focus of this talk is on understanding the role of the dopaminergic mesocorticolimbic circuit, and especially the prefrontal cortex, in higher-order executive dysfunction (e.g., disadvantageous decision-making such as trading a car for a couple of cocaine hits) in drug addicted individuals. The theoretical model that guides the presented research is called iRISA (Impaired Response Inhibition and Salience Attribution), postulating that abnormalities in the orbitofrontal cortex and anterior cingulate cortex, as related to dopaminergic dysfunction, contribute to the core clinical symptoms in drug addiction. Specifically, our multi-modality program of research is guided by the underlying working hypothesis that drug addicted individuals disproportionately attribute reward value to their drug of choice at the expense of other potentially but no-longer-rewarding stimuli, with a concomitant decrease in the ability to inhibit maladaptive drug use. In this talk I will also explore whether treatment (as usual) and 6-month abstinence enhance recovery in these brain-behavior compromises in treatment seeking cocaine addicted individuals. Promising neuroimaging studies, which combine pharmacological (i.e., oral methylphenidate, or RitalinTM) and salient cognitive tasks or functional connectivity during resting-state, will be discussed as examples for using neuroimaging in the empirical guidance for the development of effective neurorehabilitation strategies (including cognitive training) in drug addiction.

lecture

Sunday, January 28, 2018
14:30

Gerhard M.J. Schmidt Lecture Hall

Design and characterization of light-gated proteins for the investigation of medial prefrontal cortex function

Mathias Mahn (PhD Defense Thesis)

lecture

Thursday, January 25, 2018
14:00

Gerhard M.J. Schmidt Lecture Hall

Optogenetic fMRI and the Investigation of Global Brain Circuit Mechanisms

Jin Hyung Lee, PhD

Understanding the functional communication across brain has been a long sought-after goal of neuroscientists. However, due to the widespread and highly interconnected nature of brain circuits, the dynamic relationship between neuronal network elements remains elusive. With the development of optogenetic functional magnetic resonance imaging (ofMRI), it is now possible to observe whole-brain level network activity that results from modulating with millisecond- timescale resolution the activity of genetically, spatially, and topologically defined cell populations. ofMRI uniquely enables mapping global patterns of brain activity that result from the selective and precise control of neuronal populations. Advances in the molecular toolbox of optogenetics, as well as improvements in imaging technology, will bring ofMRI closer to its full potential. In particular, the integration of ultra-fast data acquisition, high SNR, and combinatorial optogenetics will enable powerful systems that can modulate and visualize brain activity in real-time. ofMRI is anticipated to play an important role in the dissection and control of network-level brain circuit function and dysfunction. In this talk, the ofMRI technology will be introduced with advanced approaches to bring it to its full potential, ending with examples of dissecting whole brain circuits associated with neurological diseases utilizing ofMRI. Short Bio: Dr. Lee received her Bachelor’s degree from Seoul National University and Masters and Doctoral degree from Stanford University, all in Electrical Engineering. She is a recipient of the 2008 NIH/NIBIB K99/R00 Pathway to Independence Award, 2010 NIH Director’s New Innovator Award, 2010 Okawa Foundation Research Grant Award, 2011 NSF CAREER Award, 2012 Alfred P. Sloan Research Fellowship, 2012 Epilepsy Therapy Project award, 2013 Alzheimer’s Association New Investigator Award, 2014 IEEE EMBS BRAIN young investigator award, and the 2017 NIH/NIMH BRAIN grant award. As an Electrical Engineer by training with Neuroscience research interest, her goal is to analyze, debug, and engineer the brain circuit through innovative technology. 1. Hyun Joo Lee†, Andrew Weitz†, David Bernal-Casas, Ben A. Duffy, Mankin Choy, Alexxai Kravitz, Anatol Kreitzer, Jin Hyung Lee*, Activation of direct and indirect pathway medium spiny neurons drives distinct brain-wide responses, Neuron, 2016;91(2):412-424. 2. Jia Liu†, Ben A. Duffy†, David Bernal-Casas, Zhongnan Fang, Jin Hyung Lee*, Comparison of fMRI analysis methods for heterogeneous BOLD responses in block design studies, Neuroimage, 2017;147:390-408. 3. David Bernal-Casas, Hyun Joo Lee, Andrew Weitz, Jin Hyung Lee*, Studying brain circuit function with dynamic causal modeling for optogenetic fMRI, Neuron, 2017;93:522-532.

lecture

Tuesday, January 23, 2018
12:30

Gerhard M.J. Schmidt Lecture Hall

Pay attention and learn from experience!: The transcriptional representation of experience and the role of the claustrum in attention

Dr. Ami Citri

conference

Tuesday, January 16, 2018
08:30 - 17:30

The David Lopatie Conference Centre

Dr. Aya Ben-Yakov

conference

Sunday, December 24, 2017
08:30 - 13:30

The David Lopatie Conference Centre

Eyal Gruntman

lecture

Monday, July 3, 2017
12:30

Gerhard M.J. Schmidt Lecture Hall

Neural Representations of Natural Self Motion: Implications for Perception & Action

Prof. Kathleen Cullen

lecture

Sunday, April 2, 2017
14:30

Gerhard M.J. Schmidt Lecture Hall

Spike based coding and computation

lecture

Tuesday, March 28, 2017
12:30

Gerhard M.J. Schmidt Lecture Hall

Could life-long memory be encoded in the pattern of holes in the Perineuronal net?

Dr. Varda Lev-Ram

Encoding of action by the Purkinje cells of the cerebellum

Prof. Reza Shadmehr

lecture

Tuesday, September 20, 2016
12:30

Gerhard M.J. Schmidt Lecture Hall

The curious case of Dr. Scoville and Mr. Molaison or: How the famous amnesic patient H.M. is not forgotten and stirs much unrest in the neuroscience community

Prof. Yadin Dudai

lecture

Sunday, September 18, 2016
12:30

Nella and Leon Benoziyo Building for Brain Research

The contribution of ventromedial prefrontal cortex to memory and decision making

Prof. Asaf Gilboa

lecture

Tuesday, September 6, 2016
12:30

Gerhard M.J. Schmidt Lecture Hall

The Self and the Friend in Space

Dr. Pia Rotshtein

Gerhard M.J. Schmidt Lecture Hall

Cognition from Action

Prof. Gyorgy Buzsaki

lecture

Tuesday, March 10, 2015
12:30

Single neurons VS. population dynamics:Which track behavior? insights from the gustatory cortex

Dr. Anan Moran

lecture

Tuesday, March 3, 2015
12:30

Gerhard M.J. Schmidt Lecture Hall

COMT*DYSBINDIN-1 CONCOMITANT REDUCTION PRODUCE SCHIZOPHRENIA-LIKE PHENOTYPES CONVERGING ON DOPAMINE PATHWAYS

Dr. Francesco Papaleo

The etiology of schizophrenia is complex and largely unknown, but consistent findings report a strong genetic component. While several potential schizophrenia-susceptibility genes have been identified, effect sizes are very small and replication is inconsistent, likely because of the complexity of human polymorphisms, genetic and clinical heterogeneity and the potential uncontrollable impact of gene-gene and gene-environment interactions. In this context, mutant mice bearing targeted mutations of schizophrenia-susceptibility genes are unique tools to elucidate the neurobiological basis of this devastating disorder. Using COMT*dysbindin-1 double mutant mice, we investigated the COMT*dysbindin-1 gene-gene interacting effects in the expression of rodents’ correlates of schizophrenia-relevant behavioral abnormalities. A major focus of our work is centered on how to dissect higher order cognitive functions in mice with high translational validity to human studies. In particular, in contrast to single genetic modifications, the combined decreased activity of both COMT and dysbindin-1 produced marked working memory, recency memory and attentional set-shifting deficits, and amphetamine supersensitivity; all abnormalities ascribed as mice’ correlates of schizophrenia-like symptoms. Based on this, we found evidence of the same non-linear genetic interaction in prefrontal cortical function in humans. Finally, to disentangle how COMT*dysbindin-1 interaction might converge in dopaminergic signaling, we measured in these double mutant mice dopamine levels in the PFC and dorsal striatum by in vivo microdialysis. Interestingly, concomitant COMT*dysbindin-1 reduction diminished dopamine levels in PFC and striatum, while amphetamine-evoked dopamine increase was attenuated in the PFC but exacerbated in the striatum. These findings illustrate a clinically relevant experimental animal model based on a predicted epistatic interaction of two schizophrenia-susceptibility genes and unravel interesting genetic mechanisms in the etiology of this mental illness.

lecture

Thursday, February 26, 2015
11:00

Gerhard M.J. Schmidt Lecture Hall

Exploring the brain's navigation system with high-resolution imaging and virtual reality

Prof. Daniel Dombeck

lecture

Thursday, February 26, 2015
12:30

Gerhard M.J. Schmidt Lecture Hall

Imaging the flow of visual information in behaving mice

Prof. Mark Andermann

lecture

Tuesday, February 24, 2015
12:30

Gerhard M.J. Schmidt Lecture Hall

Connectomes on Demand?

Prof. Nir Shavit

lecture

Wednesday, February 18, 2015
12:00

Nella and Leon Benoziyo Building for Brain Research

בין "חביון הלב" ל"טוב למות בעד ארצנו" : ייצוגי התאבדות בספרות העברית המודרנית

Maya Amitai, MD PHD

Dr. Dan Rokni

lecture

Sunday, January 4, 2015
14:30

Gerhard M.J. Schmidt Lecture Hall

lecture

Wednesday, March 5, 2014
14:30

Gerhard M.J. Schmidt Lecture Hall

From Sensory Neural Codes to Behavior

Dr. Moshe Parnas

Dr. Yossi Mandel, MD, PhD, MHA

Dr. Dina Lipkind

Small molecules against Alzheimer’s disease (AD) hallmarks and novel therapeutic targets

Dr. Abraham Fisher

Gerhard M.J. Schmidt Lecture Hall

What can parasitoid wasps teach us about decision making in the brain of insects?

Prof. Frederic Libersat

lecture

Wednesday, November 21, 2012
12:30

Gerhard M.J. Schmidt Lecture Hall

Parallel, non-convergent, interactions between separate cortical loci underlie perceptual unity: implications for a new view of object recognition

Prof. Moshe Gur

Prof. Joshua Gordon

lecture

Tuesday, April 3, 2012
12:30

Gerhard M.J. Schmidt Lecture Hall

Dr. Ilka Diester

Optogenetics is a versatile technology which is based on light sensitive membrane proteins. Those membrane proteins are called opsins. They are derived from microbial organisms which use them to orient themselves towards or away from light of specific wavelengths. Surprisingly, opsins can be safely integrated into the membranes of neurons by using viral vectors or transgenetic techniques, thus making the neurons light-sensitive without causing any aversive reaction. When shining light pulses of different wavelengths on the opsin-expressing neurons, we can either elicit or inhibit an action potential depending on the introduced opsin. Channelrhodopsin-2, for example, is an excitatory opsin which causes neurons to spike under the influence of blue light while Halorhodopsin silences neurons during the presence of yellow light. Although just six years have passed since the term optogenetics was coined, the technique quickly became one of the favorite toys of system neuroscientists. It is already used worldwide in flies, fish and rodents. Now, monkeys bring new requirements to the table. Monkeys are extremely valuable animals and are typically trained for months or years. Hence, the number of experiments with each animal is limited and each experiment has to be well planned and be conducted with exceptional care. The efforts are well justified. Monkeys resemble humans in their cognitive abilities and fine motor skills more than any other standard animal model. They can learn categories, rules and associations, come to decisions, and grasp and manipulate objects in a very human like manner. The neural correlates of these abilities are encoded in areas that are similar to human brain areas. These similarities make monkeys essential for the translation of knowledge, techniques and cures from simpler animal models, such as rodents, to humans. I will discuss recent progress in optogenetics in primates and give a glimpse on putative medical applications with a focus on bidirectional neuroprosthetic devices. Neuroprosthetics is a field which aims to help people who lost control over one or more of their limbs due to a spinal cord injury, a neural disease, a stroke, or an amputation. By reading out signals directly from cortex, decoding them, and using these decoded signals to control a prosthetic device we can bypass the faulty circuits. I will describe the opportunities which optogenetics provide for writing in tactile information. This could allow the users of neural prostheses to not only control a robotic arm but also to feel what they are grasping.

lecture

Wednesday, January 4, 2012
13:00

Gerhard M.J. Schmidt Lecture Hall

Embracing disorder: making sense of complex population codes

Dr. Omri Barak

lecture

Tuesday, January 3, 2012
13:45 - 16:30

Arthur and Rochelle Belfer Building for Biomedical Research

Dr. Iddo Magen

Prof. Kalanit Grill-Spector

Prof. Avraham Yaron

lecture

Monday, April 11, 2011
09:30 - 14:00

Gerhard M.J. Schmidt Lecture Hall

Prof. Jochen Staiger

Prof. Yaniv Assaf

Allan Kaplan

The eating disorders anorexia nervosa (AN) and bulimia nervosa (BN) are serious psychiatric disorders characterized by disturbed eating behavior and characteristic psychopathology, and in the case of AN, very low weight. The mortality of AN is the highest of any psychiatric disorder. The etiology of AN and BN are multidetermined; there are factors biologically, psychologically and socioculturallly that predispose an individual to an eating disorder. Biologically, genes contribute significantly to the risk for eating disorders. Studies have shown that the risk of anorexia nervosa in first degree relatives if one parent has AN is between 8-10%.compraed to the general population risk of 1%. The concordance rate for MZ twins in AN is close to 70%. Approximately 70% of the variance in AN is attributable to genetic effects whereas about 30% is attributable to unique environmental effects. For BN, approximately 60% of the variance in BN is attributable to genetic effects whereas about 40% is attributable to unique environmental effects. Eating disorders do not map on to one chromosome Instead there are dimensions that are genetic, such as risk of obesity, anxiety, and temperament such as perfectionism and obssessionality that are inherited and place an individual at risk for an eating disorder Gender is also a genetic risk factor for an eating disorder. Being female is a risk factor for an eating disorder, not just because females are more sensitive to cultural pressure than males. Females are more commonly affected by eating disorders because female brains are much more sensitive to dietary manipulation than male brains related to the effects of estrogen and progesterone on serotonin metabolism. Tryptophan depletion does not significantly affect levels of brain serotonin in males but dramatically reduces levels of serotonin produced in females’ brains. Dieting, especially restricting carbohydrates lowers the level of blood tryptophan available to cross the blood brain and be available to be synthesized to serotonin. Patients are at risk for an eating disorder will reduce the levels of serotonin produced in their brains by dieting and restricting carbohydrates, leading to changes in satiety and mood and increasing the likelihood of an eating disorder developing . There are those who believe that binge eating develops in response to a hyposerotonergic state in an attempt to restore tryptophan available for brain serotonin synthesis I have been involved in several large multi site genetic studies of eating disorders over the past 15 years. In a linkage analysis of affected relative AN pairs, when only restricting anorexics were included in the analyses, a significant signal was found on the long arm of chromosome 1. Candidate genes that have been found in that area of chromosome 1 include the serotonin 1D receptor gene, the opiod delta gene, and the dopamine D2 receptor gene. In a linkage analyses on a sample of affected relative pairs with BN, a significant signal was found on chromosome 10 when the sample included only subjects who vomited. I am currently involved in a whole genome wide association study ( GWAS) of 4000 AN cases and 4000 female controls which will hopefully elucidate which specific genes contribute to the risk for AN. Future genetic studies we are involved in will focus on why patients with AN are able to drop their weight to dangerously low levels, whereas patients with bulimia nervosa (BN) with similar psychopathology and dysfunctional eating behaviors are protected from extreme weight loss and do not develop AN. So far, research on genes that are important for appetite and weight regulation, such as the leptin receptor (LEPR), ghrelin (GHRL), melanocortin 4 receptor (MC4R), and brain derived neurotrophic factor (BDNF), has yielded conflicting findings in AN and BN, while related genes with potential in the same genetic systems have not been sufficiently studied. Considering that AN in adults tends to follow a chronic course and currently does not have any evidence-based treatments, determining the role of genetic factors in the vulnerability to achieve low weight in AN patients could be an important first step toward improved treatment.

lecture

Wednesday, December 29, 2010
12:00

Gerhard M.J. Schmidt Lecture Hall

On Informational Principles of Embodied Cognition

Dr. Daniel Polani

lecture

Tuesday, December 28, 2010
12:30

Jacob Ziskind Building

Visual Inference Amid Fixational Eye Movements

Dr. Yoram Burak

Our visual system is capable of inferring the structure of 2-d images at a resolution comparable (or, in some tasks, greatly exceeding) the receptive field size of individual retinal ganglion cells (RGCs). Our capability to do so becomes all the more surprising once we consider that, while performing such tasks, the image projected on the retina is in constant jitter due to eye and head motion. For example, the motion between two subsequent discharges of a foveal RGC typically exceeds the receptive field size, so the two subsequent spikes report on different regions of the visual scene. This suggests that, to achieve high-acuity perception, the brain must take the image jitter into account. I will discuss two theoretical investigations of this theme. I will first ask how the visual system might infer the structure of images drawn from a large, relatively unconstrained ensemble. Due to the combinatorially large number of possible images, it is impossible for the brain to act as an ideal observer that performs optimal Bayesian inference based on the retinal spikes. However, I will propose an approximate scheme derived from such an approach, which is based on a factorial representation of the multi-dimensional probability distribution, similar to a mean-field approximation. The decoding scheme that emerges from this approximation suggests a neural implementation that involves two neural populations, one that represents an estimate for the position of the eye, and another that represents an estimate of the stabilized image. I will discuss the performance of this decoding strategy under simplified assumptions on retinal coding. I will also compare it to other schemes, and discuss possible implications for neural visual processing in the foveal region. In the second part of the talk I will focus on the Vernier task, in which human subjects achieve hyper-acuity, greatly exceeding the receptive field size of a single RGC. The optimal decoder for this task can be formalized and analyzed mathematically in detail. I will show that a linear, perceptron-type decoder cannot achieve hyper-acuity. On the other hand a quadratic decoder, which is sensitive to coincident spiking in pairs of neurons, constitutes an effective and structurally simple solution to the problem. Furthermore, the performance achieved by such a decoder is close to the limit imposed by the ideal Bayesian decoder. Therefore, spike coincidence detectors in the early visual system may facilitate hyper-acuity vision in the presence of fixational eye-motion.

lecture

Monday, December 27, 2010
12:00

Arthur and Rochelle Belfer Building for Biomedical Research

Genetic dissection of rheumatoid arthritis – the end of the beginning

Dr. Katherine Siminovitch

lecture

Monday, December 27, 2010
15:00

Nella and Leon Benoziyo Building for Brain Research

Connectivity and activity of C. elegans locomotion

Dr. Gal Haspel

lecture

Tuesday, December 21, 2010
12:30

Jacob Ziskind Building

Optogenetic deconstruction of the neuronal circuits underlying dynamic retrieval strategies for long-term memories

Dr. Inbal Goshen

Arthur and Rochelle Belfer Building for Biomedical Research

Memory encoding and retrieval:A hippocampal “place-field centric” perspective

Prof. Etan Markus

lecture

Tuesday, May 4, 2010
12:30

Jacob Ziskind Building

Synaptic and local circuit plasticity in the dentate gyrus – potential relevance to traumatic memories

Prof. Gal Richter-Levin

lecture

Wednesday, April 28, 2010
14:30

Arthur and Rochelle Belfer Building for Biomedical Research

Neuroprotection in Multiple Sclerosis Translation of Experimental Therapy Results into Clinical Studies

Prof. Mathias Baehr

Dr. Dinu Florin Albeanu

Plasticity in high level visual cortex: insights from development and fMRI-adaptation

Dr. Kalanit Grill-Spector

The human ventral stream consists of regions in the lateral and ventral aspects of the occipital and temporal lobes and is involved in visual recognition. One robust characteristic of selectivity in the adult human ventral stream is category selectivity. Category selectivity is manifested by both a regional preference to particular object categories, such as faces, places and bodyparts, as well as in specific (and reproducible) distributed response patterns across the ventral stream for different object categories. However, it is not well understood how these representations come about throughout development and how experience modifies these representations and how do. I will describe two sets of experiments in which we addressed these important questions. First, I will describe experiments in which we examined changes in category selectivity throughout development from middle childhood (7-11 years), through adolescence (12-16) into adulthood. Surprisingly, we find that it takes more than a decade for the development of adult-like face and place-selective regions. In contrast, the lateral occipital object-selective region showed an adult-like profile by age 7. Further, recent findings from our research indicate that face-selective regions have a particularly prolonged development as they continue develop through adolescence in correlation with improved face, but not object or scene recognition memory. Development manifests as increases in the size of face-selective regions, increases in face-selectivity as well as increases in the distinctiveness of distributed response patterns to faces compared to nonfaces. Second, I will describe experiments in adults in which we examined the effect of repetition on categorical responses in the ventral stream. Repeating objects decreases responses in the human ventral stream. Repetition in lateral ventral regions manifests as a proportional effects in which responses to repeated objects are a constant fraction of nonrepeating stimuli with no change in selectivity. In contrast in medial ventral temporal cortex, we find differential effects across time scales whereby immediate repetitions produce proportional effects, but long-lagged repetitions sharpen responses, increasing category selectivity. Finally, I will discuss the implications of these results on plasticity in the ventral stream and our theoretical models linking between fMRI measurements and the underlying neural mechanisms.

lecture

Tuesday, December 15, 2009
12:30

Jacob Ziskind Building

Ongoing Dynamics and Brain Connectivity: From Intracellular Recordings to Human Neurophysiology

Dr. Amos Arieli

lecture

Tuesday, December 8, 2009
12:30

Jacob Ziskind Building

Long-term relationships between network activity, synaptic tenacity and synaptic remodeling in networks of cortical neurons

Dr. Noam Ziv

lecture

Thursday, October 29, 2009
12:30

Jacob Ziskind Building

Computational Model of Spatio-Temporal Cortical Activity in V1: Mechanisms Underlying Observations of Voltage Sensitive Dyes

Prof. David McLaughlin

Dr. Itamar Kahn

Jacob Ziskind Building

Active sensing: from natural stimulus statistics to auditory object classification in echolocating bats

Yossi Yovel

lecture

Monday, December 15, 2008
11:00

Arthur and Rochelle Belfer Building for Biomedical Research

Optogenetics: Application to Neuroscience and Neuropsychiatry

Prof. Karl Deisseroth

lecture

Sunday, December 14, 2008
14:30

Arthur and Rochelle Belfer Building for Biomedical Research

Optogenetics:Technology Development

Prof. Karl Deisseroth

Dr. Y. Peng Loh

Carboxypeptidase E (CPE) is a prohormone processing enzyme that cleaves C-terminal basic residues from peptide hormone intermediates to yield active hormones, within secretory granules of neuroendocrine cells. A transmembrane form of the enzyme has been shown to be a sorting receptor that sorts prohormones and BDNF at the trans Golgi network and targets them to the regulated secretory pathway. Recently, live cell imaging studies have demonstrated that transport of peptidergic/BDNF secretory vesicles to the release site is dependent upon CPE. The cytoplasmic tail of CPE on the vesicles binds to microtubule motors, KIF1A/KIF3A and dynein via dynactin to effect transport of prohormone/BDNF vesicles in a bidirectional manner from the soma to the process terminals and return. In addition, CPE has been found to play a neuroprotective role in adult brain. In CPE-knockout (KO) mice, degeneration of pyramidal neurons was observed in the hippocampal CA3 region of animals equal or greater than 4 weeks of age, whereas the hippocampus was intact at 3 weeks and younger. Calbindin staining indicated early termination of the mossy fibers before reaching the CA1 region, and a lack of staining of the pyramidal neurons and apical dendritic arborizations in the CA1 region of CPE-KO mice. Ex vivo studies showed that cultured hippocampal neurons transfected with an enzymatically inactive form of CPE were protected against H2O2 oxidative-stress-induced cell death but not in non-transfected or LacZ transfected neurons. Thus CPE has an anti-apoptotic role in the maintenance of survival of adult hippocampal CA3 neurons, although the mechanism of action is unknown. In hepatocellular carcinoma (HCC) cells, overexpression of CPE resulted in enhanced proliferation and migration. SiRNA knockdown of CPE expression in highly metastatic HCC cells inhibited their growth and metastasis in nude mice. These results indicate that CPE is a new mediator of tumor growth and metastasis. Thus CPE is a multi-functional protein which actions include both enzymatic and non-enzymatic to mediate various physiological functions.

lecture

Tuesday, October 7, 2008
12:15

Jacob Ziskind Building

Population imaging in vivo: from the awake to the anesthetized

Prof. Jason Kerr

lecture

Tuesday, September 23, 2008
12:15

Jacob Ziskind Building

Timing and the olivo-cerebellar system

Prof. Yosef Yarom

lecture

Tuesday, June 10, 2008
12:15

Jacob Ziskind Building

Incubation of cocaine craving: behavioral and neuronal mechanisms

Dr. Yavin Shaham

Abstract: Using a rat model of drug relapse and craving, we previously found time-dependent increases in cocaine seeking induced by exposure to drug cues after withdrawal from the drug, suggesting that cocaine craving incubates over time. In this lecture, I will first summarize our earlier behavioral and neurophysiological studies on incubation of cocaine craving. I will then discuss in more detail results from more recent studies implicating neuronal activity in the ventromedial prefrontal cortex and glutamate synaptic plasticity in the nucleus accumbens in the incubation of cocaine craving. I will also briefly address the relevance of our rat findings to the understanding of relapse to drug use in humans. Selected references related to incubation of cocaine craving Grimm JW, Hope B, Wise RA, Shaham Y (2001) Incubation of cocaine craving after withdrawal. Nature 412:141-142 Grimm JW, Lu L, Hayashi T, Su TP, Hope BT, Shaham Y (2003) Time dependent increases in brain-derived neurotrophic factor (BDNF) protein levels within the mesolimbic dopamine system following withdrawal from cocaine: implications for incubation of cocaine craving. The Journal of Neuroscience 23:742-747 Lu L, Dempsey J, Liu S, Bossert J, Shaham Y (2004) A single infusion of BDNF into the ventral tegmental area induces long-lasting potentiation of cocaine-seeking after withdrawal. The Journal of Neuroscience 24:1604-1611 Lu L, Grimm JW, Hope BT, Shaham Y (2004) Incubation of cocaine craving after withdrawal: a review of preclinical data. Neuropharmacology 47(S1): 214-227 (invited review for a special issue commemorating 30 years of NIDA research) Lu L, Hope BT, Dempsey J, Liu S, Bossert JM, Shaham Y (2005) Central amygdala ERK signaling pathway is critical to incubation of cocaine craving. Nature Neuroscience 8:212-219 Shaham Y, Hope BT (2005) The role of neuroadaptations in relapse to drug seeking. Nature Neuroscience 8:1437-1439 (special issue on Neurobiology of Addiction) Lu L, Uejima JL, Gray SM, Bossert JM, Shaham Y (2007) Systemic and central amygdala injections of the mGluR2/3 agonist LY379268 attenuate the expression of incubation of cocaine craving. Biological Psychiatry 61:591-598 Koya E, Uejima J, Wihbey K, Bossert JM, Hope BT, Shaham Y (2008) Role of ventral medial prefrontal cortex in incubation of cocaine craving. Neuropharmacology (in press, for a special issue commemorating 35 years of NIDA research)) Conrad KL, Tseng K, Uejima J, Reimers J, Heng L, Shaham Y, Marinelli M, Wolf ME (2008) Formation of accumbens GluR2-lacking AMPA receptors mediates incubation of cocaine craving. Nature (in press)

lecture

Thursday, June 5, 2008
13:30

Arthur and Rochelle Belfer Building for Biomedical Research

Single- and Double-Opponent Neurons in Primary Visual Cortex, and Their Different Roles in Color Perception

Prof. Robert Shapley

lecture

Tuesday, June 3, 2008
12:15

Jacob Ziskind Building

Pain Selective Anesthesia

Dr. Alex Binshtok

Prof. Chaya Kalcheim

Prof. Leszek Kaczmarek

Prof. Larry Abbott

lecture

Monday, January 14, 2008
13:00

Arthur and Rochelle Belfer Building for Biomedical Research

Can economics learn something from measuring time response?

Prof. Ariel Rubinstein

lecture

Tuesday, December 4, 2007
12:15

Jacob Ziskind Building

Trying to make sense of the cerebellum: models and experiments

Dr. Opher Donchin

lecture

Tuesday, November 20, 2007
12:15

Jacob Ziskind Building

The accessory olfactory (vomeronasal) system: a sensory adapted for social interactions

Dr. Shlomo Wagner

lecture

Tuesday, November 13, 2007
14:30

Nella and Leon Benoziyo Building for Brain Research

Clarifying the functional neuro-anatomy of face processing by combining lesion studies and neuroimaging

Prof. Bruno Rossion

When is it worth working: Behavioral, physiological, genetic, and modeling experiments investigating motivation and reward expectancy

Dr. Barry J. Richmond

The intensity or vigor of goal-directed behavior is a correlate of the motivation underlying it. Motivation is related to the subjective value of rewards and is moderated, or even completely dissipated, if the perceived effort or discomfort seems too great. Under what circumstances do we seek a goal or a reward? To study motivated behavior in monkeys, we use several variants of a task in which monkeys must perform some work, in this case detecting when a target spot turns from red-to-green, to obtain a drop of juice. We use another visual stimulus, a cue, to indicate how much discomfort must be endured, e.g., the number of trials to be worked, to obtain the reward. The monkeys learn about the cues quickly, often after just a few trials. The number of errors becomes proportional to amount of work remaining before reward, achieving our goal of manipulating motivation. This is a behavior in which the monkeys decrease their performance in response to an increased predicted workload. Temporal difference models have provided an important framework for interpreting goal directed-behavior, and in economics, game theory has been used to model choice behavior. A key concept in these models is to determine how the value of the reward is modulated by some parameter of the experiment, such as changing the reward size, or the amount of time needed to obtain the reward. In learning or adaptation the TD algorithm predicts that behavior should be (and in artificial systems is) adapted to maximize long-term reward. By examining the influence of reward size, waiting time, and amount of work, we can examine in what ways different model succeed and fail. Our data show that performances depend on work completed since preceding reward (sunk cost effect), and accumulated reward (over whole sessions) and work. In addition this behavior can be used to learn about categorization and rule learning. Using single neuronal recording, regional ablation, and molecular ablation of the D2 receptor we show that dopamine-rich brain regions have signals related to the balance between reward and work.

lecture

Tuesday, January 2, 2007
12:00 - 13:15

Nella and Leon Benoziyo Building for Brain Research

Stress and the Brain – a Molecular View

Dr. Daniela Kaufer

lecture

Monday, January 1, 2007
12:00

Nella and Leon Benoziyo Building for Brain Research

Synaptic maintenance - Insights from live imaging experiments

Dr. Noam Ziv

All events

Computational trade-offs as a core principle of brain function

Unlocking the Night: Novel Approaches Advancing the Neuroscience of Sleep and Cognition

Trauma Under Psychedelics: How trauma during altered states of consciousness impacts cognitive, physiological, neural, and clinical outcomes

Cognitive processing in the cerebellum

What is special about activity in the basal ganglia?

Network models for memory storage with biologically constrained synapses: implications for representational drift.

Cell type dependent computations and learning in primary motor cortex

Information processing in the vomeronasal system

Deciphering the role of the DCC/UNC-40 receptor in dopaminergic neurons during health and disease

The Evolution and Plasticity of the CONNECTOME

Neuromodulation of experience-dependent sexually dimorphic learning

The Computational and Neural Basis of Cognitive Dynamics and Diversity

Anatomical organization of the human hippocampal system

The Neural Basis of Affective States

Perceptual decision coding is inherently coupled to action in the mouse cortex

Deep language models as a cognitive model for natural language processing in the human brain

Anterior-Posterior Insula Circuit Mediates Retrieval of a Conditioned Immune Response in Mice

"Hot and Cold Thoughts"

Neuroprotective and Anticonvulsant Effects of Cannabinoids with Neurotrauma

The Evolution of 7T (and Beyond) MRI in Basic Research and Clinical Practice

The role of neurons in the direction-selective retinal circuit in visual processing in the retina and in the visual thalamus

Designing Language Models to Think Like Humans

This decision, not just the average decision: Factors contributing to one single perceptual judgment

Reading Minds & Machines-AND-The Wisdom of a Crowd of Brains

Memory and Obliviscence:From Random to Structured Material

Elucidating convergence and divergence of neural mechanisms: from genes to behavior

Memory consolidation and generalization during sleep

Blood flow perturbations and its impact on brain structure and function: from microstrokes to heartbeats

Vasosdynamics of cortical arterioles and what it informs us about neuronal activity

The evolution and development of critical periods of cortical plasticity

Consciousness and the brain: comparing and testing neuroscientific theories of consciousness

Beyond Touch: Exploring Audible Aspects of Rodent Whisking

Information processing in spiking networks: Converging assemblies

Studying Ageing and Neurodegenerative Brain with Quantitative MRI

Hippocampal pathology and pathophysiology in the development of temporal lobe epileptogenesis

Dimensionality bottleneck uncovers simple action selection rules in hunting zebrafish

A brain-computer interface for studying long-term changes of hippocampal neural codes

Travelling waves or sequentially activated modules: mapping the granularity of cortical propagation

Mapping the world around us: A topology-preserved schema of space that supports goal-directed navigation

The role of the corpus callosum in interhemispheric communication

Mechanistic insights into ‘brainwashing’

One molecular- and one circuit-level insight into cognition from studying Drosophila

Non-canonical circuits for olfaction

Immunoception: Brain Representation and Control of Immunity

Olfactory information processing: timing, sequences, geometry and relevance

A paradigm shift in GPCR recruitment and activity: GPCR Voltage Dependence Controls Neuronal Plasticity and Behavior

Context-Dependent Dynamic Coordination of Head and Eye Movements During Visual Orienting

Dissecting the role of peripheral immunity in Alzheimer’s Disease pathogenesis and disease course

Experience-dependent genetic and synaptic regulation of stability and plasticity in cortical circuits

Understanding spontaneous neuronal activity with neurophotonics

Germ-cell migration and fate maintenance in zebrafish

Dendritic voltage imaging, excitability rules, and plasticity

Chromatin 3D distribution in live muscle nuclei: impacts on epigenetic activation/repression of chromatin

Toward “reading” and “writing” neural population codes in the primate cortex

Mood temporal dynamics characterized with computational and engineering-based approaches

Beyond the arcuate fasciculus: A multiplicity of language pathways in the human brain

Reprogramming the topology of the nociceptive circuit in C. elegans reshapes sexual behavior

Local and long-range inputs contributing to sequence generation in the zebra finch

Volatile cortical working memory representations crystalize with practice

Cognitive neuroscience of learning and memory in human infants

The neurocircuit underlying social approach and avoidance behavior

Illuminating neural computations with structured light and sound wavefronts

Features and Objects as Perceptual Attractors: Theory, Paradigm, and Results from The Rat’s Whisker System

Smell and our unconscious sense of self

An Innate Immunity Pathway Against Invading Microbes Targets the Paternal Mitochondria for Destruction after Fertilization

Nature, nurture, and the neuroscience of parenthood

Nature, nurture, and the neuroscience of parenthood

Correlated light and electron microscopy reveal recurrent circuit motives in the zebrafish hindbrain visual integrator network

Navigation in larval zebrafish:strategies and internal representations

The neurobiological function of experience-regulated genomic enhancers From transcriptional mechanisms to control over synaptic plasticity and sensory processing

Neuronal activity and noise in synaptic wiring specificity

Deciphering integration of contradictory signals in epithelial-to-mesenchymal transition

Horizontal cells of the vertebrate retina – From channels to functions

Sensory processing in the whisker system of awake, behaving mice

How the brain transforms sensory input into action

Cerebral Cortex Connectomics

Mapping brainstem nuclei structure and connectivity in health and disease

Active vision and vision for action

Representation of 3D space in the mammalian brain:From 3D grid cells in flying bats to 3D perception in flying humans