Past events | The department of Brain Sciences

All events, All years

Measuring Behavior and Physiology: Bridging the Genotype Phenotype Gap

Conference

Date:

Thursday, March 3, 2011

Hour: 08:00 - 16:30

Location:

Dolfi and Lola Ebner Auditorium

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Stimulus-specific adaptation – beyond the oddball paradigm

Lecture

Date:

Tuesday, March 1, 2011

Hour: 12:30

Location:

Jacob Ziskind Building

Prof. Israel Nelken

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Dept of Neurobiology Hebrew University of Jerusalem

Stimulus-specific adaptation is the decrease in the responses to a common stimulus that does not generalize, or generalize only partially, to other stimuli. Stimulus-specific adaptation in the auditory modality has been studied mostly with oddball sequences, which consist of a common and a rare stimuli. Recently, we started to use a number of other sound sequences in order to study the properties of adaptation in auditory cortex. I will show that (1) SSA is not only the result of the adaptation of the response to the common stimulus - in addition, the responses to the rare tones have a component due to the deviance of the rare tone relative to the regularity set by the common tone; (2) neuronal responses in auditory cortex of rats show sensitivity to finer types of statistical regularities; and (3) SSA can be evoked by other sounds as well, including sounds as similar to each other as two tokens of white noise. These results suggest the existence of a highly sensitive 'statistical machine' that analyzes and interprets the auditory scene.

Deletion of the mouse genomic interval corresponding to human 16p11.2 causes autism-like phenotypes

Lecture

Date:

Wednesday, February 23, 2011

Hour: 15:00

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Guy Horev

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Postdoctoral Fellow Cold Spring Harbor Laboratory

Autism is a neuro-cognitive disorder characterized by a broad spectrum of clinical features including repetitive behaviors, restricted interests, language impairment, and altered social interactions. Although chromosome rearrangements affecting specific genomic intervals have been found in patients with autism, the basis for this syndrome is unknown. Deletion of 16p11.2 has been associated with autism, and patients with this deletion have a wide range of clinical symptoms. Here we used chromosome engineering to generate mice with deletion of the 27 genes corresponding to those affected in autism patients with 16p11.2 deletion, as well as mice harboring duplication of the same region. Mice with decreased dosage of this region have unique phenotypes including neonatal lethality, alterations in the volumes of specific brain regions, as well as behaviors reminiscent of clinical features of autism. In particular, mice with 16p11.2 deletion showed behaviors that were repetitive and restricted to specific locations, in contrast to diploid controls that showed a gradual increase in freedom of movement under similar conditions. These findings provide the first functional evidence that compromised dosage of 16p11.2 is causal in autism.

Pavlovian-like behavior in microbes

Lecture

Date:

Tuesday, February 22, 2011

Hour: 12:30

Location:

Jacob Ziskind Building

Prof. Yitzhak (Tzachi) Pilpel

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Department of Molecular Genetics, WIS

The ability to anticipate and prepare in advance to changes in the environment is ascribed to neuronal systems in multi-cellular organisms. Yet by means of gene expression regulatory connectivity microbes too may have evolved to "anticipate" and prepare in advance. I will present evidence for microbial Pavlovian-like conditioning and discuss the similarities and differences to conditioning in the neuronal-cognitive context.

Mechanisms of vocal learning in the songbird: A hypothesis for the role of cortical-basal ganglia circuits

Lecture

Date:

Monday, February 21, 2011

Hour: 12:30

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Michale Fee

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Dept of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA

Young songbirds, like humans, learn their vocalizations by imitating their parents. This process happens in a series of stages. After memorizing the song of an adult tutor, young birds begin to babble, singing highly random variable sounds. By listening to their own sounds and comparing them with the memory of the tutor song, they gradually refine their song until it can be a nearly exact copy of the tutor. How all this happens at the level of neural circuitry is not yet clear, but recent experiments have begun to shed light on the brain regions and mechanisms involved in the generation of babbling and exploratory variability, in the evaluation of the song, and in the implementation of corrective plastic changes in the motor circuitry. I will describe our current hypothesis for how interacting cortical-basal ganglia circuits implement these various processes underlying vocal learning.

Unraveling the structure of time in the brain

Lecture

Date:

Sunday, February 20, 2011

Hour: 11:00

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Michale Fee

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Dept of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA

Whether we are speaking, swimming, or playing the piano, we are crucially dependent on our brain?s capacity to step through sequences of neural states. Songbirds provide a marvelous animal model in which to study this phenomenon. Their stereotyped vocalizations have hierarchical temporal structure spanning two orders or magnitude in timescale ? from individual vocal gestures lasting ten milliseconds, to song syllables (~100 msec), to song motifs (~1 sec). Several brain areas have been proposed to control timing at these different timescales. By manipulating these circuits with temperature change and observing the effect on song structure, we have been able to localize a single ?clock? circuit in the premotor vocal pathway. Intracellular neuronal recordings during singing elucidate the mechanism by which this clock circuit operates. Our findings are consistent with the predictions of a synfire-chain model? a synaptically connected chain of neurons in HVC. Our findings are inconsistent with models in which subthreshold dynamics, such as ramps or oscillations, play a role in the control of timing.

A sensorimotor account of phenomenal consciousness

Lecture

Date:

Wednesday, February 16, 2011

Hour: 11:00

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. J Kevin O'Regan

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Laboratoire Psychologie de la Perception CNRS - Université Paris Descartes

The problem of consciousness is sometimes divided into two parts: An "easy" part, which involves explaining how one can become aware of of something in the sense of being able to make use of it in one's rational behavior. This is called access consciousness. And a "hard" part, which involves explaining why sensations feel like something, or have a kind of sensory presence, rather than having no feel at all. This is called phenomenal consciousness. Phenomenal consciousness is considered hard because there seems logically no way physical mechanisms in the brain could explain such facts. For example why does red look red, rather than looking green, or rather than sounding like a bell. Indeed why does red have a feel at all? Why do pains hurt instead of just provoking avoidance reactions? The sensorimotor approach provides a way of answering these questions by appealing to the idea that feels like red and pain should not be considered as things that happen to us, but rather as modes of ineraction with the environment. I shall show how the idea can be applied to color, touch, pain, and sensory substitution. In addition to helping understand human consciousness, the approach has applications in virtual reality and in robotics.

New Insights on Structural Neuroplasticity from MRI

Lecture

Date:

Tuesday, February 15, 2011

Hour: 12:30

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Yaniv Assaf

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Dept. of Neurobiology Tel Aviv University

Neuro-plasticity is one of the key processes in our brain's physiology. This process allows our brain to change itself, functionally and structurally, following the acquisition of a new skill or experience. While functional aspects of neuro-plasticity can be studied using non-invasive techniques such as fMRI, EEF and MEG, investigation of the structural tissue characteristics of neuro-plasticity requires invasive histological approaches. Long-term experience necessitates structural plasticity which, in the adult brain, is characterized by changes in the shape and number of the synapses (synaptogenesis) as well as other process (neurogenesis, gliogenesis and white matter plasticity). Structural MRI studies of brain plasticity reveal significant volumetric changes via voxel-based morphometry of T1 weighted scans. Yet, the micro-structure correlates of these changes are not well understood. Diffusion tensor imaging (DTI) became one of the most popular imaging techniques in neuroimaging and is regarded as a micro-structural probe. Recently, tract-based spatial statistics (TBSS) analysis of DTI scans before and after long-term motor coordination training (juggling) revealed regional fractional anisotropy (FA) increase in parietal pathways. In that study, FA changes were reported following few weeks of training. An open question is what happens at shorter term learning and memory processes? In a short term spatial navigation study performed both in humans and rodents, we found that diffusion MRI can detect structural changes in cell morphology induced by plasticity within mere hours. Both in humans and rodents, the micro-structural changes, as observed by MRI, were localized to the anticipated brain regions: hippocampus, para-hippocampus, visual cortex, cingulate cortex and insular cortex. Our results indicate that significant structural occur in the tissue within mere hours - an interesting result by itself from the neurophysiological point of view. However, by investigating the induced structural changes both by histology and MRI it is possible to elucidate the relations between tissue micro-structure and the diffusion MRI signal. Preliminary results of such comparison indicate that in gray matter tissue one of cellular correlates of diffusion MRI indices is the density and shape of astrocyte. Indeed more studies should be directed

A new, "sensorimotor", view of seeing

Lecture

Date:

Monday, February 14, 2011

Hour: 14:00

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. J Kevin O'Regan

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Laboratoire Psychologie de la Perception CNRS - Université Paris Descartes

There seem to be numerous defects of the eye that would be expected to interfere with vision. Examples are the upside down retinal image, the blind spot in each eye's visual field, non-uniform spatial and chromatic resolution, and blur and image shifts caused by eye saccades. In order to overcome such defects scientists have proposed a variety of compensation mechanisms. I will argue that such compensation mechanism not only face empirical difficulties, but they also suffer from a philosophical objection. They seem to require the existence of a "homunculus" in the brain that contemplates the picture-like output of the compensation mechanism. A new view of what "seeing" consists in is required. The new view of seeing considers seeing as a particular way of actively exploring the environment. This "sensorimotor" approach is subtly different from the idea of "active vision" known today in cognitive or computer science. The sensorimotor approach explains how, despite the eye's imperfections and despite interruptions in the flow of sensory input, we can have the impression of seeing everything in the visual field in detail and continuously. I shall show how the phenomenon of "inattentional blindness" (or "Looked but Failed to See") is expected from the new approach, and I shall examine the phenomenon of "change blindness" which arose as a prediction from the theory. Finally I examine the question of the photographic quality of vision: why we have the impression of seeing things all over the visual field, why everything seems simultaneously and continuously present, and why things seem to visually impose themselves upon us in a way quite different from how memory and imagining do. To explain these facts I shall invoke four objectively measurable aspects of visual interactions: richness, bodiliness, partial insubordinateness and grabbiness.

Reconfiguring Memory

Lecture

Date:

Sunday, February 13, 2011

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Shuli Sade

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Artist, NYC

: Sadé will talk about the relevance in collaboration between artists and scientists, and will introduce her recent art project: “Reconfiguring Memory”. Sadé collaborates with Professor Andre Fenton at NYU Neuroscience labs to develop art for the renovated Neuroscience labs at NYU. Her work with memory, time and light led to this collaboration and will result in art relating to the questions: How does the brain store experience as memories and how the expression of knowledge activates information that is relevant without activating what is irrelevant, and what visual methods can be used for recording the activity of memory, gain or loss.

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All events, All years

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.

On Informational Principles of Embodied Cognition

Lecture

Date:

Wednesday, December 29, 2010

Hour: 12:00

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Daniel Polani

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School of Computer Science, University of Hertfordshire, UK

For many decades, Artificial Intelligence adopted a platonic view that intelligent behaviour is produced in the "brain" only and any body is only an incidental translator between thought and action. In the last two decades, in view of the successes of the subsumption architecture and embodied robotics, this perspective has changed to acknowledge the central importance of the body and the perception-action loop as whole in helping an organisms' brain to carry out useful ("intelligent") behaviours. A central keyword for this phenomenon is, of course, "environmental/morphological computation" (Paul 2006; Pfeifer and Bongard 2007). The question arises, how/why exactly does this work? What are the principles that make environmental computation work so successfully and how can the contribution that the body provides to cognition be characterized objectively? In the last years, Information Theory has been identified as providing a natural language to characterize cognitive processing, cognitive invariants as well as the contribution of the embodiment to the cognitive process. The talk will review some highlights of the current state-of-the-art in the field and provide some - sometimes quite surprising - illustrations of the power of the informational view of cognition.

Visual Inference Amid Fixational Eye Movements

Lecture

Date:

Tuesday, December 28, 2010

Hour: 12:30

Location:

Jacob Ziskind Building

Dr. Yoram Burak

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Center for Brain Science, Harvard University

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.

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

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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

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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

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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

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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

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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

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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.