All events, All years

Can economics learn something from measuring time response?

Lecture
Date:
Tuesday, December 11, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Ariel Rubinstein
|
School of Economics, Tel Aviv University & Dept of Economics, New York University

The lecture will use the results about time response (see Rubinstein (2007), http://arielrubinstein.tau.ac.il/papers/78.pdf ) to discuss the potential meaning of the neuroeconomics approach to economics. Before the lecture please respond to the 15min questionnaire posted at: http://gametheory.tau.ac.il/student/poll.asp?group=1391

Trying to make sense of the cerebellum: models and experiments

Lecture
Date:
Tuesday, December 4, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Opher Donchin
|
Department of Biomedical Engineering Ben Gurion University, Beer Sheva

In this talk I will describe a recent controversy that has arisen regarding the intrinsic properties of Purkinje cells and explain the importance of this controversy to our understanding of Cerebellar function. In brief, it has been shown that Purkinje cell membrane potential is bistable, but there remains significant disagreement about whether this bistability has a functional role. In our lab, we addressed the controversy by recording from Purkinje cells in an awake animal and testing to see whether bistability that had been observed in vitro and in anaesthetized animals could also be seen in a behaving animal. Our findings will not settle the controversy, nor settle the question of the Cerebellum's functional role, but they will significantly shift the terms of the debate. We found that all of the predictions we tested confirmed the potential for a functional role for Purkinje cell bistability. This will force a serious re-evaluation of our understanding of Cerebellar circuitry.

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

Lecture
Date:
Tuesday, November 20, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Shlomo Wagner
|
Dept of Biology and Dept of Neurobiology and Ethology, Haifa University

Many mammals rely on pheromones to mediate social interactions. Traditionally pheromones were thought to be detected by the accessory olfactory (vomeronasal) system, but recent studies indicated a central role for the main olfactory system in this function. Thus, unraveling the functional difference between these two chemosensory systems is essential for understanding pheromone-mediated social interactions. In this study we show that mitral cells of the accessory olfactory bulb respond to sensory input in a bimodal manner: a transient response is elicited by low level stimulation, whereas strong stimuli evoke sustained firing that lasts for 10-30 s. This is in sharp contrast to the unimodal response of main olfactory bulb mitral cells. We further show that this difference is dictated by distinct membrane properties of the two neuronal populations. We hypothesize that, via its sustained activity, the accessory olfactory system induces a new sensory state in the animal, reflecting its social context.

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

Lecture
Date:
Tuesday, November 13, 2007
Hour: 14:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Bruno Rossion
|
University of Louvain, Belgium

Understanding the functional neuro-anatomy of face processing in the human brain is a long-standing goal of Cognitive Neuroscience. Up to the early 90’s, the most important source of knowledge was from lesion studies, i.e. making correlations between the localization of lesions in groups of brain-damaged patients and their face recognition impairments. The influence of the cognitive approach in Neuropsychology, with an emphasis on single-case functional investigations, as well as the advent of neuroimaging studies in the healthy brain, have considerably reduced the importance of lesion studies in clarifying the neuro-anatomical aspects of face processing. In this talk, my goal will be to illustrate how neuroimaging investigations of single-cases of acquired prosopagnosic patients can still greatly increase our knowledge in this field. Neuroimaging studies of the normal brain have shown that the middle fusiform gyrus (‘FFA’) and the inferior occipital gyrus (‘OFA’) are activated by both detection and identification of faces. Among other observations, our studies of the patient PS, a case of prosopagnosia with normal object recognition, show that the right ‘FFA’ can be recruited to detect faces independently of the ‘OFA’ of the same hemisphere (Rossion et al., 2003). However, fMRI-adaptation investigations suggest that both areas are necessary to perform individual discrimination of faces (Schiltz et al., 2006). Recent observations also show that the the same brain area, here the right ‘FFA’, may be impaired at individual face discrimination while performing normal individual object discrimination. This suggests that clusters of neurons coding specifically for different categories in this area (Grill-Spector et al., 2006) can be functionnally independent. Finally, when structurally intact, non-face preferring areas such as the ventral part of the lateral occipital complex (vLOC) may subtend residual individual discrimination of faces following prosopagnosia. Altogether, these studies show that faces are processed through multiple pathways in the human brain, with a subset of these areas responding preferentially to faces being critical for efficient face recognition.

Compulsive Rats and Compulsive Humans

Lecture
Date:
Tuesday, November 13, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Daphna Joel
|
Dept of Psychology, Tel Aviv University

Obsessive-compulsive disorder (OCD) is a psychiatric disorder affecting 1-3% of the population. Although several brain regions have been implicated in the pathophysiology of OCD, including the basal ganglia-thalamo-cortical circuits and the dopaminergic and serotonergic systems, the ways in which these neural systems interact to produce obsessions and compulsions in patients is currently unknown. Moreover, although to date, there are effective pharmacological and behavioral treatments to OCD, many patients do not respond to these treatments. For obvious reasons, the understanding and treatment of diseases such as OCD, must rely heavily on appropriate animal models that closely mimic their behavioral and if possible their neural manifestations. We have recently developed a new rat model of OCD, in which ‘compulsive’ lever-pressing is induced by the attenuation of an external feedback of this behavior. Compulsive lever-pressing is abolished by selective serotonin reuptake inhibitors, but not by anxiolytic antipsychotic, and non-serotonergic antidepressant drugs, in accordance with the differential efficacy of these drugs in alleviating obsessions and compulsions in OCD patients. Compulsive lever-pressing is also sensitive to manipulations of the orbitofrontal cortex and of the dopaminergic and serotonergic systems, in line with different lines of evidence implicating these systems in the pathophysiology of OCD. The model is used to screen new pharmacological agents with anti-compulsive activity; to map brain regions in which high frequency stimulation exerts an anti-compulsive effect; to test the autoimmune hypothesis of OCD; to assess the role of genetic vulnerability in OCD; to unravel the role of female gonadal sex hormones in compulsive behavior; and to uncover the neural mechanisms of OCD

Molecular Mechanisms for the Initiation and Maintenance of Long Term Memory Storage

Lecture
Date:
Tuesday, November 6, 2007
Hour: 15:00
Location:
Dolfi and Lola Ebner Auditorium
Prof. Eric Kandel
|
Prof., Columbia University, NY Sr Investigator, Howard Hughes Medical Institute

Alzheimers disease amyloid plaques: Tombs or time bombs? Lipids induce release of neurotoxic oligomers from inert amyloid fibrils

Lecture
Date:
Tuesday, October 30, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Inna Kuperstein
|
Center of Human Genetics, Flanders Institute & KU, Leuven, Belgium

Alzheimer's disease (AD) is associated with the aggregation of Amyloid-beta peptide (Aβ). It is more and more believed that neurotoxicity is caused during the Aβ aggregation process, by soluble Aβ oligomers species, and not by the Aβ fibrils themselves that considered as inert end-products of the aggregation process. Nevertheless, stability of Aβ fibrils might be overestimated. We found that inert Aβ fibrils can be reversed to toxic oligomers in the presence of synthetic phospholipids and lipid rafts components as gangliosids, sphingomyelin and cholesterol. Interestingly, the equilibrium is not shifted towards monomeric Aβ but rather towards soluble amyloid oligomers (backward oligomers). Biochemical and biophysical analysis reveals that backward oligomers are very similar to the oligomers found during the classical aggregation process of monomeric Aβ (forward oligomers). Backward oligomers cause synaptic markers loss and immediate neurotoxicity to primary neurons followed by apoptotic cell death. In addition, mice brain icv. injection of backward amyloid oligomers causes Tau phosphorylation, Caspase 3 activation and memory impairment in mouse similarly to forward oligomers. Finally, we observe that release of toxic oligomers and subsequent neurotoxicity may be caused by other disease-associated amyloid peptides as TAU, Prion 1 and synthetic amyloidogenic peptide in the presence of lipids. We propose that lipid-induced fibrils disassembly and release of soluble oligomers is a common generic mechanism of amyloids. An important implication of our work is that amyloid plaques are not inert and should be considered as potential large reservoirs of neurotoxic oligomers that can rapidly be mobilized by lipids. Although lipid metabolism has been implicated in neurodegenerative diseases the precise involvement of lipids in basic toxicity mechanisms in AD is a major question. Our data could help to understand this Aβ and lipid relationship in more detail.

Understanding Exploratory Behavior

Lecture
Date:
Tuesday, October 23, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Ilan Golani
|
Dept of Zoology, Tel Aviv University

Unlike the situation in neurophysiology, where the relevant variables are mostly known, it is not clear what is to be measured in the study of behavior; what is a reliable datum? What are the elementary patterns? To highlight the building blocks of movement and their organization we use 4 tools: (i) we study gradients: along the body dimension, in space and in time (in moment-to-moment behavior, ontogeny, and recovery). Gradients provide natural origins of axes for measurement, reveal how building blocks are gradually added on top of each other to form the animal's full repertoire, and unite seemingly disparate behaviors into continua. (ii) We systematically change coordinate systems, to find the ones highlighting invariant features. We use multiple kinematic variables to describe the behavior. They may or may not cluster into discrete patterns. (iii) We study behavior on more than one scale. For example, along the body dimension we use 2 scales that of the path, and that of multi-limb coordination. Finally, (iv) we segment movement using intrinsic geometrical and statistical properties. By using combinations and conjunctions of the elementary building blocks we work our way up from low level to cognition- and motivation-related constructs. In my talk I will describe how these tools are implemented in a bottom-up study of mouse (Mus musculus) and fly (Drosophila melanogaster) exploratory behavior.

Linear and non-linear fluorescence imaging of neuronal activity

Lecture
Date:
Wednesday, September 19, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Jonathan Fisher
|
Howard Hughes Medical Institute, The Rockefeller University, New York

Benoziyo Center for Neurological Diseases-Third Annual Symposium

Conference
Date:
Sunday, September 9, 2007
Hour:
Location:

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"A Functional Circuit Underlying Male Sexual Behaviour Uncovered in

Lecture
Date:
Sunday, July 8, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Tali Kimchi
|
Dept of Molecular & Cellular Biology, Howard Hughes Medical Institute, Cambridge, MA

Integrate & Play Theory of Hippocampal Function:

Lecture
Date:
Monday, July 2, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Dori Derdikman
|
Centre for the Biology of Memory Norwegian University of Science & Technology (NTNU) Trondheim, Norway

An alternative model to the Declarative-Memory & Cognitive Map theories of the function of the hippocampus is suggested. the new model may explain the deficits described in the famous case of H.M., who displayed total anterograde amnesia following a surgery in which a bilateral dissection of the whole medial-temporal lobe (MTL) was perfromed (Scoville and Milner, 1957) . According to the model, the main functions of the MTL are: (1) to act as an integrator (2) to detect novelty. The integrator function is used, for example, for generation of the place-cell and grid-cell system. Normally, the MTL is integrating an episode until it detects a novel situation. Once the MTL detects such a novel situation, it sends the executive brain (perhaps the basal ganglia and/or prefrontal cortex) a message that it is time to play a novel behavioral game. In the case of H.M., where the MTL is missing, the executive brain never gets the message that an episode is novel, and thus continues to play "old games". In principle, at least, if this model is correct, H.M. could be cured from his memory problem, if the executive brain would have received the missing novelty signals artificially.

Itch more than scratching the surface

Lecture
Date:
Monday, June 25, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Gil Yosipovitch
|
Dept of Dermatology, Neurobiology & Anatomy, & Regenerative Medicine, Wake Forest University Health Sciences Winston-Salem, NC

Predicting odor pleasantness from odor structure:Pleasantness as a reflection of the physical world

Lecture
Date:
Monday, June 18, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Noam Sobel
|
Dept of Neurobiology, WIS

The cell biology of Alzheimer's disease: Intracellular pathways to pathogenesis

Lecture
Date:
Monday, June 11, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Scott A. Small
|
Columbia University, School of Physicians and Surgeons, New York, NY

The Hippocampus and Memory: Consolidation or Transformation?

Lecture
Date:
Tuesday, May 29, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Gordon Winocur
|
Rotman Research Institute, Toronto, Ontario, Canada

Adaptation and integration in the multimodal space map of the barn owl

Lecture
Date:
Monday, May 21, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Yoram Gutfreund
|
Dept of Physiology & Biophysics, Faculty of Medicine, Technion, Haifa

Linking Network Archtecture to Neural Coding in the Olfactory System

Lecture
Date:
Monday, May 7, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Roni Jortner
|
Interdisciplinary Center for Neural Computation Hebrew University of Jerusalem and Computation and Neural Systems, California Institute of Technology

Learning induces new representations of instructions and actions in the motor cortex

Lecture
Date:
Monday, April 30, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Eilon Vaadia
|
Dept of Physiology, Faculty of Medicine, The Hebrew University of Jerusalem

Structural analysis of serotonin transporter mechanism and regulation

Lecture
Date:
Wednesday, April 18, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Gary Rudnick
|
Dept of Pharmacology Yale University School of Medicine

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