All events, 2007

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:

Homepage

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

Common mechanisms mediate synapse formation during development and synapse plasticity during learning and memory

Lecture
Date:
Monday, July 30, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Samuel Schacher
|
Center for Neurobiology & Behavior, Columbia University College, New York, NY

Pages

All events, 2007

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

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

Common mechanisms mediate synapse formation during development and synapse plasticity during learning and memory

Lecture
Date:
Monday, July 30, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Samuel Schacher
|
Center for Neurobiology & Behavior, Columbia University College, New York, NY

"The Effects of Age-Related Morphologic Changes

Lecture
Date:
Sunday, July 29, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Doron Kabaso
|
Department of Biomathematical Sciences Mount Sinai School of Medicine, New York, NY, USA

Pages

All events, 2007

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All events, 2007

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