Past events | The department of Brain Sciences

All events, All years

Ode To Memory A mini-series devoted to memory in cinema

Lecture

Date:

Tuesday, January 18, 2011

Hour: 14:00

Location:

Dolfi and Lola Ebner Auditorium

Prof. Yadin Dudai

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Dept of Neurobiology, WIS

A cellular mechanism for general enhancement of learning capability

Lecture

Date:

Tuesday, January 18, 2011

Hour: 12:30

Location:

Jacob Ziskind Building

Dr. Edi Barkai

|

University of Haifa

Learning-related cellular modifications occur not only at synapses but also in the intrinsic properties of the neurons. Learning-induced enhancement in neuronal excitability is evident in hippocampal and piriform cortex pyramidal neurons following a complex olfactory-discrimination operant conditioning task. Such enhanced excitability is manifested in reduced spike frequency adaptation that results from reduction in the slow afterhyperpolarization (AHP), which develops after a burst of action potentials. AHP reduction is apparent throughout the pyramidal cells neuronal population. The AHP amplitude tends to return back to its initial value within days when training is suspended. This recovery is accompanied by reduced learning capability, but not by loss of memories for learned odors. The post-burst AHP reduction is mediated by decreased conductance for a specific calcium-dependent potassium current, the slow IAHP. This long-lasting reduction is dependent on persistent activation of the PKC and ERK second messenger systems. Similar long-lasting AHP reduction can be induced in-vitro by repetitive synaptic stimulation or by kainate application. Such activity-dependent AHP reduction is occluded by prior learning. Olfactory-learning induced enhanced neuronal excitability in CA1 pyramidal neurons is also accompanied by enhanced learning capability in a novel hippocampus-dependent task, the Morris water maze. We suggested that AHP reduction is the cellular mechanism that enables neuronal ensembles to enter into a state which may be best termed "learning mode". This state lasts for up to several days and its behavioral manifestation is enhanced learning capability in tasks that depend on these particular neuronal ensembles. Specifically, enhanced neuronal excitability sets a time window in which most neurons in the relevant neuronal network are more excitable, and thus activity-dependent synaptic modifications are more likely to occur.

What the brain knows about what’s in the nose: Neural processing of pheromone signals

Lecture

Date:

Monday, January 17, 2011

Hour: 12:30

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Dr. Yoram Ben-Shaul

|

Harvard University

Understanding the neuronal events linking sensory inputs with behavioral outputs in complex organisms is a central goal of neuroscience. First steps in this enormous endeavor can be made by focusing on the relatively simple and stereotyped class of chemosensory triggered innately encoded physiological processes. Until recently, analysis of the circuits that underlie these processes was hampered by the lack of a reliable method for stimulus delivery to the vomeronasal system, which in mice, like many other mammals, plays a key role in processing pheromonal information. To address this issue, I developed an experimental preparation that allows in-vivo stimulus delivery to the mouse vomeronasal system and combined it with multisite neuronal recordings to measure stimulus evoked neuronal activity. Recordings from the early processing stage of the accessory olfactory bulb reveal the broad range and high acuity of ethologically relevant sensory representations, and furthermore suggest that these involve integrative processing. Recording from subsequent processing relays in the vomeronasal amygdala reveal several similarities to the olfactory bulb representations but also some intriguing differences raising new hypotheses about the role of the amygdala in these processes. Finally, I will describe how I am extending this approach by employing optogenetic techniques to record neuronal activity from scarce and genetically defined neurons in subsequent processing regions. Taken together, these experiments are beginning to illuminate the function of entire neuronal circuits involved in mediating ethologically and clinically relevant endocrine processes.

Topographic mapping of a hierarchy of temporal receptive windows using natural stimuli

Lecture

Date:

Thursday, January 13, 2011

Hour: 12:00

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Uri Hasson

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Dept of Psychology, Princeton University

Space and time are two fundamental properties of our physical and psychological realms. While much is known about the integration of information across space within the visual system, little is known about the integration of information over time. Using two complementary methods of functional magnetic resonance imaging (fMRI) and intracranial electroencephalography (iEEG), I will present evidences that the brain uses similar strategies for integrating information over space and over time. It is well established that neurons along visual cortical pathways have increasingly large spatial receptive fields. This is a basic organizing principle of the visual system: neurons in higher-level visual areas receive input from low level neurons with smaller receptive fields and thereby accumulate information over space. Drawing an analogy with the spatial receptive field (SRF), we defined the temporal receptive window (TRW) of a neuron as the length of time prior to a response during which sensory information may affect that response. As with SRFs, the topographical organization of the TRWs is distributed and hierarchical. The accumulation of information over time is distributed in the sense that each brain area has the capacity to accumulate information over time. The processing is hierarchical because the capacity of each TRW increases from early sensory areas to higher order perceptual and cognitive areas. Early sensory cortices such as the primary auditory or visual cortex have relatively short TRWs (up to hundreds of milliseconds), while the TRWs in higher order areas can accumulate information over many minutes.

Multimodal interactions in primary auditory cortex: Laminar dependence & modulation by general anesthetics

Lecture

Date:

Tuesday, January 11, 2011

Hour: 12:30

Location:

Jacob Ziskind Building

Prof. Matthew I. Banks

|

University of Wisconsin, USA

Current theories of the neural basis of sensory awareness suggest that neocortex is constantly comparing expected with observed sensory information. This comparison arises through the integration of ascending inputs from the sensory periphery and descending cortical inputs from the same or other sensory modalities. The importance of this integrative process for awareness is suggested by its selective loss upon anesthetic-induced hypnosis and during slow-wave sleep, but how this integration and its disruption by anesthetics occur within a cortical column is unclear. Using electrophysiological and imaging techniques in rodents in vivo and in brain slices, we show that extrastriate visual cortex provides descending input to primary auditory cortex that modulates responses to auditory stimuli, and that the integration of these information streams is disrupted by general anesthetics.

A Neural Mechanism for Reasoning and Believing

Lecture

Date:

Wednesday, January 5, 2011

Hour: 15:30

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Michael Shadlen

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Physiology and Biophysics Dept University of Washington

Spatial Memory, Healthy Cognition and Successful Aging

Lecture

Date:

Wednesday, January 5, 2011

Hour: 12:00

Location:

Nella and Leon Benoziyo Building for Brain Research

Prof. Veronique Bohbot

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Faculty of Medicine McGill University, Quebec, Canada

Young healthy participants spontaneously use different strategies in a virtual radial maze, an adaptation of a task typically used with rodents. We have previously shown using fMRI that people who use spatial memory strategies have increased activity in the hippocampus whereas response strategies are associated with activity in the caudate nucleus. In addition, we used Voxel Based Morphometry (VBM) to identify brain regions co-varying with the navigational strategies individuals used. Results showed that spatial learners have significantly more grey matter in the hippocampus and less grey matter in the caudate nucleus than response learners. The relationship between spatial memory strategies and grey matter of the hippocampus was replicated with healthy older adults. Furthermore, we found a positive correlation between spatial memory strategies and the MoCA, which is a test sensitive to mild cognitive impairment. Since low grey matter in the hippocampus is a risk factor for cognitive deficits in normal aging and for Alzheimer’s disease, our results suggest that using spatial memory in our everyday lives may protect against degeneration of the hippocampus and associated cognitive deficits These results have important implications for intervention programs aimed at healthy and successful aging.

Visual Inference by Composition

Lecture

Date:

Tuesday, January 4, 2011

Hour: 12:30

Location:

Jacob Ziskind Building

Prof. Michal Irani,Prof. Michal Irani

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Dept of Computer Science and Applied Mathematics, WIS

In this talk I will show how complex visual tasks can be performed by exploiting redundancy in visual data. Comparing and integrating data recurrences allows to make inferences about complex scenes, without any prior examples or prior training. I will demonstrate the power of this approach to several visual inference problems (as time permits). These include: 1. Detecting complex objects and actions (often based only on a rough hand-sketch of what we are looking for). 2. Summarizing visual data (images and video). 3. Super-resolution (from a single image). 4. Prediction of missing visual information. 5. Detecting the "irregular" and "unexpected". 6. "Segmentation by Composition".

The Optimism Bias: A tour of the positively irrational brain

Lecture

Date:

Thursday, December 30, 2010

Hour: 15:00

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Tali Sharot

|

University College London

New Developments in the Genetics of Eating Disorders

Lecture

Date:

Wednesday, December 29, 2010

Hour: 15:00

Location:

Nella and Leon Benoziyo Building for Brain Research

Allan Kaplan

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Professor of Psychiatry, University of Toronto

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.

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All events, All years

Connectivity and activity of C. elegans locomotion

Lecture

Date:

Monday, December 27, 2010

Hour: 15:00

Location:

Nella and Leon Benoziyo Building for Brain Research

Dr. Gal Haspel

|

National Institute of Neurological Disorders and Stroke, NIH

I study the neuronal basis of locomotion in the nematode C elegans. With only 302 neurons in its nervous system, 75 of which are locomotion motorneurons, C. elegans offers a tractable network to study locomotion. In this talk I will describe my research, which uses a neuroethological approach to study both the behavior and the underlying connectivity and activity of neurons and muscle cells.

Genetic dissection of rheumatoid arthritis – the end of the beginning

Lecture

Date:

Monday, December 27, 2010

Hour: 12:00

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Dr. Katherine Siminovitch

|

Mount Sinai Hospital Toronto, Ontario

In this talk I will review the rationale for searching for autoimmune disease susceptibility genes and in particular for genes conferring risk for rheumatoid arthritis(RA). I will then review the current state of knowledge on RA genes and will then focus on one of the few newly-discovered genes (PTPN22) for which we know the disease causal gene variant. This gene encodes a tyrosine phosphatase ,LYP, and I will present recent data from my lab in which we use an animal model to show how the RA-associated PTPN22/LYP variant causes T cell dysfunction that could predispose to autoimmunity.

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

Lecture

Date:

Tuesday, December 21, 2010

Hour: 12:30

Location:

Jacob Ziskind Building

Dr. Inbal Goshen

|

Dept of Bioengineering, Stanford University, Stanford CA

Cognitive function and emotional homeostasis, and the aspiration to decipher their neuronal basis have stood at the heart of neuroscience since its inception. The complexity of the circuits underlying these processes is immense, and new techniques are necessary to provide novel efficient ways to make a significant progress in brain research. Optogenetic tools enable temporally and spatially precise in-vivo activation or inactivation of genetically defined cell populations, thus enabling deconstruction of systems that were not available for research. An example for that is my work re-examining the role of the hippocampus in remote memory. The prevailing theory suggests that the process of remote memory consolidation requires early involvement of the hippocampus, followed by the neocortex. In the course of this process, an influence of hippocampus on neocortex may enable the hippocampus to facilitate the remote cortical storage of memory, rather than stably store the memory itself. Indeed, contextual fear memories in rodents are completely unaffected by hippocampal lesions or pharmacological inhibition on the remote timescale of weeks after training, but do depend on the hippocampus over the recent timescale of days after training. However, in exploring the contribution of defined cell types to remote memory using optogenetic methods (which are orders of magnitude faster in onset and offset than earlier methods), we found that even weeks after contextual conditioning, the contextual fear memory recall could be abolished by optogenetic inhibition of excitatory neurons in the CA1 region of the hippocampus- at times when all earlier studies had found no detectable influence of hippocampus. We also optogenetically confirmed the remote-timescale importance of anterior cingulate cortex. In exploring mechanisms, we found that loss of hippocampal involvement at remote timepoints depended on the timescale of hippocampal inhibition, since 1) we replicated earlier pharmacological work using longer-lasting drug-mediated inhibition of hippocampus (revealing the recent, but not remote, effects on memory); and 2) extending optogenetic inhibition of hippocampus to match typical pharmacological timescales converted the remote hippocampus-dependence to remote hippocampus-independence. These findings uncover a remarkable dynamism in the mammalian memory retrieval process, in which underlying neural circuitry adaptively shifts the default structures involved in memory—normally depending upon the hippocampus even at remote timepoints, but flexibly moving to alternate mechanisms when the hippocampus is offline on the timescale of minutes. This new model is further supported by the finding that contextual memory was instantaneously suppressed by CA1 inhibition even in the midst of a single freely-moving behavioral session, after the memory was already retrieved. Our findings have broad implications for the interpretation of drug or lesion data in other systems, and may open an exciting therapeutic avenue for PTSD patients, in which a pathology-inducing contextual memory could be stopped as it appears without permanently affecting other memories.

Anesthesia: a window to the neuronal activity underlying consciousness

Lecture

Date:

Tuesday, December 7, 2010

Hour: 12:30

Location:

Jacob Ziskind Building

Dr. Aeyal Raz

|

Dept of Anesthesia Rabin Medical Center

The neural mechanisms underlying consciousness have been one of the most intriguing yet elusive questions facing science. We will discuss how the activity of the neuronal population changes during loss of consciousness following administration of general anesthesia drugs. We measured the changes of Sub-thalamic nucleus neurons activity during administration of propofol (GABAA agonists) and Remifentanil (opiate agonist). This was done during implantation of deep brain stimulation electrodes for the treatment of Parkinson’s disease in humans. Administration of both Propofol and remifentanil leads to a similar reduction of STN multi-unit neuronal spiking activity. Remifentanil seems to interfere with the oscillatory pattern of STN activity whereas propofol does not. In order to broaden our understanding of the effect of anesthetic drugs, we performed extra-cellular recordings of neuronal activity from the cortex and globus pallidus of vervet monkeys using multiple electrodes. The recordings were performed during sedation with Ketamine (NMDA antagonist). Our results demonstrate the appearance of synchronous oscillatory activity of the LFP at slow (<1 Hz) delta (3-4Hz) and gamma (35-50Hz) in the motor cortex and globus pallidus following ketamine injection and loss of consciousness. These oscillations are synchronized between regions as well, and are correlated to the spiking activity of neurons in these regions. We propose that loss of consciousness following anesthesia is due to the appearance of synchronized oscillatory activity in different regions of the brain, preventing the normal processing and passage of information.

Acquired alternative splicing changes in Alzheimer's and Parkinson's diseases

Lecture

Date:

Tuesday, November 30, 2010

Hour: 12:30

Location:

Jacob Ziskind Building

Prof. Hermona Soreq

|

Safra Center of Neuroscience The Hebrew University of Jerusalem

Multiple lines of evidence link numerous diseases to inherited errors in alternative splicing, the process connecting different exon and intron sequences to diversify gene expression. We explore potential involvement of acquired alternative splicing changes in non-familial Alzheimer's and Parkinson's diseases (AD, PD), where synaptic functioning fails and cholinergic or dopaminergic neurons die prematurely. Using whole genome microarrays, we found massive decline in exon exclusion events in the AD entorhinal cortex. In brain-injected mice, blocking exon exclusion caused learning and memory impairments and destruction of cholinergic neurons caused AD-like changes in exon exclusion. Suggesting physiological relevance, blocking exon exclusion in primary neuronal cells was preventable by cholinergic stimulation and caused dendritic and synapse loss. In comparison, blood leukocytes from advanced PD patients showed different alternative splicing changes. These were largely reversed by deep brain stimulation (DBS), which reduces motor symptoms, and were reversed again after disconnecting the stimulus. Measured modifications correlated with neurological treatment efficacy and classified controls from advanced PD patients and pre- from post-surgery patients. In an independent patient cohort, a "molecular signature" (6 out of the modified transcripts) further classified controls from patients with early PD or other neurological diseases. Our findings demonstrate functionally relevant disease-specific alternative splicing changes in the AD brain and PD leukocytes; highlight acquired alternative splicing changes as causally involved in different neurodegenerative diseases and identify new targets for intervention in DBS-treatable neurological diseases.

Visualizing Circuits in the Visual System

Lecture

Date:

Thursday, November 25, 2010

Hour: 12:00

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Josh Sanes

|

Center for Brain Science Harvard University

Formation of neural circuits requires that axons recognize appropriate cells, and even appropriate parts of cells, upon which to synapse. In the retina, amacrine and bipolar cells form synapses on retinal ganglion cells (RGCs) in the inner plexiform layer (IPL). The visual features to which different RGC subtypes respond depend on what input they receive, prime determinants of which are the IPL sublaminae in which their dendrites make synapses. We have therefore sought molecules that mark RGC subtyoes and mediate lamina-specific connectivity. Candidates include members of the immunoglobulin superfamily, such as Sidekicks, Dscams and JAMs, and members of the cadherin superfamily, such as Class II and protocadherins. I will discuss our progress toward identifying and testing such candidates. I will also discuss methods for tracing connections of retinal neurons in wild-type and mutant mice, so that we can assess the consequences of perturbing target recognition systems.

Cortical blood flow: Every (subsurface) vessel counts

Lecture

Date:

Wednesday, November 24, 2010

Hour: 11:00

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. David Kleinfeld

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Dept of Physics University of California at San Diego La Jolla, CA

Neuronal processing has a high energetic cost, all of which is supplied through brain vasculature. What are the design rules for this system? How is flow controlled by neuronal activity? How do neurons respond to failures in the vasculature? Theses questions will be addressed at the level of necortex in rat and mouse. An essential aspect of this work is the use of nonlinear optical tools to measure and perturb vasodynamics and automate the large-scale mapping of brain angioarchitecture.

The neurobiology of seizures and depression

Lecture

Date:

Tuesday, November 23, 2010

Hour: 12:30

Location:

Jacob Ziskind Building

Dr. Oscar G. Morales

|

Associate Director, Psychiatric Neurotherapeutics Program (PNP) Harvard Medical School

Altered Function of the Prefrontal Cortex Following Extended Access to Self-Administered Cocaine

Lecture

Date:

Monday, November 8, 2010

Hour: 13:30

Location:

Nella and Leon Benoziyo Building for Brain Research

Dr. Osnat Ben-Shahar

|

Dept of Psychology University of California Santa Barbara

One main alteration in neural function observed in human cocaine addicts is reduced function in the medial prefrontal cortex (mPFC). However, whether altered function of the mPFC precede, or result from, excessive self-administration of cocaine, and the exact neurochemical changes it consists of, is still unknown. To answer these questions, one needs an appropriate animal model of addiction. As, it is well established that differences in the route of, and control over, cocaine-administration, or in the frequency and size of the daily-dose of cocaine, result in significant differences in cocaine-induced neurochemical effects; then if we are to better understand the neuroadaptations that underlie the development of addiction in humans, we should employ animal models that mimic as closely as possible the human situation. Hence, my lab utilize an animal model that employs intravenous self-administration of cocaine, under conditions (based on Ahmed & Koob, 1998) that distinguish the effects of brief versus extended daily access to cocaine upon both behavior and neural substrates. This permits the investigation of neuroadaptations associated with the transition from the drug-naïve state to controlled drug-use, versus the further adaptations associated with the transition from controlled to compulsive drug-use. Using this model, we measured basal, as well as cocaine-induced, release of glutamate and dopamine within the mPFC during and after various levels of exposure to cocaine. The differences we found between controlled and compulsive drug-states, will be discussed in this talk.

HOW RHYTHMIC ACTIVITIES IN THE BRAIN MAKE YOU FEAR AND FORGET

Lecture

Date:

Tuesday, October 12, 2010

Hour: 12:30

Location:

Jacob Ziskind Building

Prof. Hans-Christian Pape

|

Institute for Physiology I Westfälische Wilhelms University Münster, Germany

Fear is a crucial adaptive component of the behavioral repertoire that is generated in relation to stimuli which threaten to perturb homeostasis. Fear-relevant associations are learned and consolidated as part of long term memory. After learning, fear responses are modulated through processes termed safety learning and extinction. Perturbation of these mechanisms can lead to disproportional anxiety states and anxiety disorders. Recent years have seen considerable progress in identifying relevant brain areas – such as the amygdala, the hippocampus and the prefrontal cortex - and neurophysiological principles. Key mechanisms, involving rhythmic oscillations of neuronal subpopulations and neuromodulatory influences, will be discussed