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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Entorhinal grid cells and hippocampal memory

Lecture
Date:
Tuesday, February 27, 2007
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Edvard I. Moser
|
Director, Centre for the Biology of Memory, Norwegian University of Science and Technology, Trondheim, Norway

Representation in entorhinal grid cells

Lecture
Date:
Monday, February 26, 2007
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. May-Britt Moser
|
Co-director, Centre for the Biology of Memory, Norwegian University of Science and Technology, Trondheim, Norway

Structural and functional changes induced by prenatal stress

Lecture
Date:
Monday, February 19, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Marta Weinstock-Rosin
|
Department of Pharmacology, The Hebrew University of Jerusalem

Adaptive mechanisms in the auditory system

Lecture
Date:
Monday, February 12, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Merav Ahissar
|
Department of Psychology, Faculty of Social Sciences, The Hebrew University of Jerusalem

The mechanisms underlying our remarkable ability to form coherent and meaningful percepts in our complex environment are still an unresolved mystery. I propose that fast adaptive processes occurring at all levels of the processing hierarchy play a major role in this ability. I will give examples from speech perception and from tone comparison. A unique population in this respect are individuals with reading and learning disabilities. Their adaptive stimulus-specific mechanisms are impaired, with broad perceptual and cognitive consequences.

Molecular crossroads of neuronal plasticity and neuropathology

Lecture
Date:
Wednesday, February 7, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Natalia V. Gulyaeva
|
Deputy Director, Inst. of Higher Nervous Activity & Neurophysiol, Moscow Russia

Imaging synaptic development and plasticity of adult-born neurons in the mouse Olfactory Bulb

Lecture
Date:
Monday, February 5, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Adi Mizrahi
|
Department of Neurobiology, The Hebrew University of Jerusalem

The mammalian brain maintains few developmental niches where neurogenesis persists into adulthood. One niche is located within the olfactory system where the olfactory bulb (OB) continuously receives newborn neurons that integrate into the network as functional interneurons. However, little is known about the mechanisms of development and function of this unique population. In this study, we set out to directly image newborn neurons and synapses by combining high resolution in vivo two-photon microscopy and lentivirus labeling. Overexpressing cytosolic GFP or a synaptic protein (PSD95-GFP) reveals the general dendritic structure and/or synaptic distributions along dendritic trees, respectively. In vivo imaging reveals the dynamic behavior of dendrites and synapses over time. Adult-born neurons were transduced at the subventricular zone and imaged in the OB where they start to mature into functional neurons. First, time-lapse imaging of newborn neurons over several days revealed that dendritic formation is highly dynamic with distinct dynamics for spiny neurons and non-spiny neurons. The dynamic nature of newborn development was not affected by sensory deprivation. Once incorporated into the network, adult-born neurons maintain significant levels of structural dynamics. This structural plasticity is local, cumulative and sustained in neurons several months after their integration. Second, synapse formation on these young cells and dendrites was verified by EM analysis of PSD95-GFP expressing cells. Using these neurons we found that early during development, synaptic distributions are highly ordered along dendritic trees. Third, these synapses continuously change locations along dendritic shafts as revealed time-lapse imaging over several days. Interestingly, these newborn neurons remain structurally dynamic months after they have been incorporated into the network. I will also discuss preliminary results where we use in vivo calcium to decipher the physiological activity of unique populations in the OB and cortex. These experiments provide an experimental model to directly study the dynamics of neuronal and synaptic development in the intact mammalian brain and provide direct evidence for the ongoing plasticity of the adult-born neuronal population.

Structure and dynamics of neuronal networks: impact on representation

Lecture
Date:
Monday, January 29, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Shimon Marom
|
Dept of Physiology, Faculty of Medicine, Technion

The structure of large random networks is explored using spontaneous and evoked activities recorded from a subset of individual neurons. The emerging topology is that of a complex dynamic graph. Impacts on concepts of representation are analyzed.

Spatial processing in the auditory brainstem-new roles for synaptic inhibition

Lecture
Date:
Thursday, January 25, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Benedikt Grothe
|
Ludwig Maximilians University, Munich, Germany

The arrival times of a sound at the two ears are only microseconds apart, but both birds and mammals can use these interaural time differences to localize low-frequency sounds. Traditionally, it was thought that the underlying mechanism involved only coincidence detection of excitatory inputs from the two ears. However, recent findings have uncovered profound roles for synaptic inhibition in the processing of interaural time differences. In mammals, exquisitely timed hyperpolarizing inhibition adjusts the temporal sensitivity of coincidence detector neurons to the physiologically relevant range of interaural time differences. Inhibition onto bird coincidence detectors, by contrast, is depolarizing and devoid of temporal information, providing a mechanism for gain control.

Conflict resolution: a monkey fMRI study

Lecture
Date:
Tuesday, January 23, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Maria de la O Olmedo Babe
|
Brain Research Institute, University of Bremen, Germany

fMRI is a technique that allows us to observe brain function; from a small group of neurons to the whole brain and from attentional or perceptual basic mechanisms to high executive functions. Conflict resolution is an executive function that allows to process constantly new information and react according to the needs of the situation. Stroop, Simon and Flanker effects in humans are well described in the literature (Stroop, 1935, Pardo, 1990, Wittfoth, 2006). In order to investigate the neural bases, two monkeys were trained in tasks that involve conflict resolution. Stimulus arrangement was chosen such as to investigate Stroop, Simon and Flanker effects by analyses of behavioral and imaging data.

Computational physiology of the high frequency discharge and pauses of basal ganglia neurons

Lecture
Date:
Monday, January 15, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Hagai Bergman
|
Department of Physiology, Faculty of Medicine, The Hebrew University of Jerusalem

The neurons of many basal ganglia nuclei, including the external and internal globus pallidus (GPe, GPi respectively) and the substantia nigra pars reticulta (SNr) are characterized by their high-frequency (50-100 spikes/s) tonic discharge (HFD). However, the high firing rate of GPe neurons is interrupted by long pauses. To provide insight into the GPe pause physiology, we developed an objective criterion for the quality of the isolation of extracellularly recorded spikes and studied the spiking activity of 212 well-isolated HFD GPe and 52 GPi/SNr neurons from five monkeys during different states of behavioral activity. An algorithm which maximizes the surprise function was used to detect pauses and pauser-cells ("pausers"). Only 6% of the GPi/SNr neurons vs. as many as 56% of the GPe neurons were classified as pausers. The average pause duration equals 0.6s and follows a Poissonian distribution with a frequency of 13 pauses/minute. No linear relation was found between pause parameters (duration or frequency) and the firing rate of the cell. Pauses were preceded by various changes in firing rate but not dominantly by a decrease. The average amplitude and duration of the spike waveform was modulated only after the pause but not before it. Pauses of pairs of cells which were recorded simultaneously were not correlated. The probability of GPe cells to pause spontaneously was extremely variable among monkeys (30-90%) and inversely related to the degree of the monkey's motor activity. These findings suggest that spontaneous GPe pauses are neither triggered by an intrinsic cellular mechanism nor by slow global changes in the extracellular medium and probably reflect a network property of the basal ganglia related to low-arousal and network exploration periods.

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