All events, All years

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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Ca2+-Activated Currents in Mouse Gonadotrophs

Lecture
Date:
Thursday, September 6, 2007
Hour: 10:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Dennis W. Waring
|
Division of Endocrinology, Dept of Medicine, University of California, CA

Playing with sounds: How echolocating bats solve different approach tasks

Lecture
Date:
Wednesday, August 15, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Mariana Melcon
|
Animal Physiology Section, Tubingen University, Germany

Hippocampal place cell representation of the environment: To remap or not to remap? That is the question

Lecture
Date:
Monday, August 13, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Etan Markus
|
Dept of Psychology, Behavioral Neurosciences Division, University of Connecticut, Storrs, CT

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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

Auditory self-perception and gating in a songbird

Lecture
Date:
Tuesday, April 17, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Richard Hahnloser
|
Institute of Neuroinformatics, UZH/ETHZ, Zurich

Vocal production and learning rely on the evaluation of auditory feedback. We use the songbird as a model system for exploring how auditory feedback in vocalizing animals is represented by auditory brain areas, and how auditory signals are gated back into premotor areas involved in song production and learning. We expose juvenile zebra finches to distorted auditory feedback and record from neurons in field L, an avian forebrain area thought to be analogous to mammalian primary auditory cortex. Most field L neurons in our ongoing study do not respond to auditory perturbation during singing, despite their motor-related firing being similar to auditory responses to playback of the bird’s own song. We argue that this behaviour of field L neurons is reminiscent of mirror neurons in primate inferior frontal cortex. In adult birds, we demonstrate modulation and gating of auditory and spontaneous cerebral activity by the thalamic nucleus uveaformis (Uva): The normal dependence of premotor-like spike patterns (bursts) on the behavioural state can be reversed by pharmacological manipulation of Uva activity. Our results show that avian thalamic relay neurons have a function that is reminiscent of a mixture of functions attributed to relay and reticular neurons in the mammalian thalamus. In summary, our findings of corollary motor discharges in auditory brain areas and of explicit thalamic gating mechanisms help to advance the understanding of auditory feedback processing and sensorimotor integration for complex learned behaviors.

guilt by association: Memory context effects, source memory, and the frontal lobes

Lecture
Date:
Monday, April 16, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Daniel Levy
|
Gonda Brain Research Center, Bar-Ilan University & Dept of Neurobiology, WIS

As in many domains of cognition, the effects of context on memory are ubiquitous and pervasive. Even memory-impaired neurological patients and aging individuals with deficits in direct source recollection benefit from context reinstatement during retrieval. Though context effects on free and cued recall are robust, findings regarding context effects on recognition have been widely divergent. We have proposed a multifactorial model of context effects that takes into account the impact of hippocampally-based target-context binding, anterior medial temporal lobe-based additive familiarity, and frontal lobe-based strategic processes that suppress response bias to acheive mnemonic advantages. I will discuss findings from simulations and neuropsychological studies of the elderly that illustrate these factors. I will also present new data that suggest differences between temporal and spatial context and discuss their implications for memory models.

Epigenetic mechanisms in memory formation

Lecture
Date:
Sunday, April 15, 2007
Hour: 12:00 - 13:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. David Sweatt
|
Head, Neurobiology Dept and Mcknight Brain Institute, University of Alabama, Birmingham AL

Dr. Sweatt's seminar will focus on molecular mechanisms underlying learning and memory. Dr. Sweatt uses knockout and transgenic mice to investigate signal transduction mechanisms in the hippocampus, a brain region known to be critical for higher-order memory formation in animals and humans. His talk will describe transcriptional regulation in memory formation, focusing on studies of transcription factors, regulators of chromatin structure, and other epigenetic mechanisms, in order to understand the role of regulation of gene expression in synaptic plasticity and memory.

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