All events, 2016

Dissecting striatal circuits in learning and decision making

Lecture
Date:
Thursday, January 28, 2016
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Ilana Witten
|
Princeton Neuroscience Institute, NJ

I will describe two lines of work in mice aimed at dissecting the role of neuromodulation in the striatum in regulating reward-related learning and decision making. The first story addresses the question of how dopaminergic neurons that innervate the striatum support both learning and action generation, with results suggesting that distinct subpopulations of dopamine neurons support each function. The second story identifies a role for cholinergic interneurons in the ventral striatum in the formation of reward-context associations, with results pointing to a potent ability of the cholinergic neurons in regulating behaviorally-relevant plasticity.

Sensory mechanisms of long-distance navigation in birds

Lecture
Date:
Sunday, January 17, 2016
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Dmitry Kishkinev
|
Research Fellow, School of Biological Sciences, Queen's University Belfast, Northern Ireland, UK

Displacement studies have clearly showed that birds are able to perform true navigation, i.e. they can find direction leading to destination from unfamiliar territory. Yet, the sensory mechanisms of navigation remain poorly understood. There are two primary hypotheses explaining the sensory nature of navigation: (1) a magnetic map hypothesis proposes that birds use parameters of the geomagnetic field which predictably distributed on the globe. This hypothesis claims that the magnetic receptor cells used for navigation reside in the upper beak (the so-called ‘beak organ’), and transmit information via the trigeminal nerve to the brain; (2) an olfactory map hypothesis assumes that birds can use olfaction and smell their position by taking advantage of odours predictably distributed in the atmosphere. In the last decade, I together with my co-workers have experimentally tested both hypotheses in migratory songbird species by combining sensory manipulations with displacements both in Europe and North America. Specifically, in our main model species, Eurasian reed warblers (Acrocephalus scirpaceus), a long-distance nocturnal migrant, we have found that this species (and maybe other songbird migrants) use geomagnetic cues and the magnetoreceptors embedded in the trigeminal system for geographical positioning. In parallel with our studies, there is a growing support for olfactory long-distance navigation in sea birds and homing pigeons. In my talk, I will overview the challenges of understanding true navigation in birds and present the most important advances in the context of other relevant studies.

Reprogramming in vivo neural circuits by engineering new synaptic connections

Lecture
Date:
Wednesday, January 13, 2016
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Ithai Rabinowitch
|
Fred Hutchinson Cancer Research Center, Seattle USA

Synaptic connections between neurons are a fundamental building block of neural circuits. They determine circuit function, and shape whole animal behavior. In order to understand the causal role of synapses in regulating circuit function I have developed a novel synaptic engineering approach that consists of genetically inserting new electrical synapses between specified neurons in vivo. I have successfully implemented this technique in C. elegans circuits and have used it in a variety of applications. For example, for revealing a coincidence detecting mechanism in a nose-touch circuit, for switching olfactory preferences from attraction to a favorable odor into aversion, and for investigating a cross-modal mechanism that compensates for the loss of one sense by sharpening another. Synaptic engineering is thus a powerful new approach that should be widely applicable to a range of animals, enabling to probe, modify and potentially also repair neural circuits. In the long run interventional techniques such as synaptic engineering could make it possible to “upgrade” the nervous system.

PKA signaling network: Visualizing through Macromolecular Assembly and High Resolution Imaging of the Brain

Lecture
Date:
Tuesday, January 12, 2016
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Ronit Ilouz
|
Dept of Pharmacology, University of California San Diego

cAMP dependent Protein kinase (PKA) plays a critical role in numerous neuronal functions including neuronal excitability, synaptic plasticity, learning and memory. Specificity in PKA signaling is achieved in part by the four functionally non-redundant regulatory (R) subunits. The inactive holoenzyme has a dimeric R subunit bound to two Catalytic (C) subunits. The full-length holoenzyme crystal structures allow me to understand how isoform-specific assembly can create distinct holoenzyme structures that each defines its allosteric regulation. High-resolution large-scale mosaic images provide global views of brain sections and allow identification of subcellular features. Analysis of multiple regions demonstrates that the R isoforms are concentrated within discrete regions and express unique and consistent patterns of subcellular localization. Using the miniSOG technique for correlating fluorescent microscopy with electron microscopy I find RIβ in the mitochondria within the cristae and the inner membrane, and in the nucleus, modifying the existing dogma of cAMP-PKA in the nucleus. Down-regulation of the nuclear RIβ, but not RIIβ, decreased L-LTP related signaling as reported by CREB phosphorylation in primary neuronal cultures, consistent with deficits observed in RIβ knockout mice. Furthermore, we show that a point mutation in the RIβ gene, that is associated with a neurodegenerative disease, abolishes dimerization while retaining robust interaction with the catalytic subunit. As a consequence, the interaction with an A-Kinase Anchoring Protein (AKAP) was also diminished. This mutation abolishes the AKAP-mediated targeting of RIβ holoenzymes to specific cellular compartments, which is consistent with an accumulation of RIβ in neuronal inclusions in patients carrying this mutation. These diverse interdisciplinary tools are defining PKA signaling as highly localized complexes that are targeted to specific sites in the cell in close to proximity to substrates and other signaling molecules where activity is then regulated by local levels of cAMP and calcium as well as kinases and phosphatases.

Representation of motion in hierarchical neural systems

Lecture
Date:
Tuesday, January 5, 2016
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Avner Wallach
|
Faculty of Health Sciences, University of Ottawa, Canada

The vertebrate nervous system evolved a highly complex hierarchical architecture. While considerable progress has been made in describing the representation of behaviorally relevant state-variables by high-level circuits, how these circuits interact with low-level networks and modulate behavior is still poorly understood. In this talk I will describe two studies that begin to address this issue by exploring the transformations of motion representation across different tiers of the neural hierarchy. In the first study, conducted at Ehud Ahissar's lab at the Weizmann Institute of Science, we explored the generation and processing of rhythmic phase coding, previously reported as a key state-variable in cortical processing of rodent vibrissal perception. Using closed-loop motion control in anesthetized rats, we found that the vibrissal mechanoreceptors generate this invariant phase representation, which is then differentially processed by the various secondary brainstem populations. In the second study, underway in Leonard Maler's lab at the University of Ottawa, we focus on the preglomerular complex (PG) of the weakly electric fish Apteronotus leptorhynchus. This small, densely packed diencephalic structure serves as an exclusive gateway from the hindbrain and midbrain circuits to the telencephalon, which is involved in memory formation and spatial navigation. We found both spatial and temporal compression of motion related information conveyed through the PG bottleneck, suggesting an effective 'division of labor' between the low and high levels of the hierarchy.

Novel optical tools for controlling plasticity and unique Photoactivatable Ca2+ probes for targeted imaging

Lecture
Date:
Monday, January 4, 2016
Hour: 14:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Shai Berlin
|
Dept of Molecular & Cell Biology & Helen Wills Neuroscience Institute University of California, Berkeley

Neuronal plasticity is a unique property that describes the ability of the system to undergo long-lasting changes, typically as a result of experience. This paradigm, initially discovery by Bliss and Lomo and dubbed long term potentiation (LTP), describes a scenario where the post-synaptic responses increase in strength for long durations, following a particular pre-synaptic stimulus. Conversely, LT-Depression, describes the long lasting depression of synaptic responses. Today, these phenomena are commonly used to describe the molecular model for learning and memory. A large body of work has implicated more than a hundred proteins and factors in modulating LTP and LTD, and thereby memory. Unfortunately, there is still a lively debate regarding the true necessity and exact role of each player. The need for new techniques and approaches to further explore synaptic function and dysfunction has never been more pressing, as the number of people developing neurodegenerative diseases rises exponentially to epidemic scales, with the aging population. These diseases are characterized by a strong decline in the number of synapses and in the ability of synapses to undergo plasticity, ultimately resulting in the severe decline of cognitive function- such as learning and memory. To better scrutinize synaptic plasticity and probe the function and role of its initiators (i.e. NMDA receptors and calcium ions), I have developed novel light-gated NMDA receptors and photoactivatable fluorescent Ca2+-probes to monitor synaptic activity with unmet spatio-temporal resolution and reversibility. I use the latter to examine the roles of specific NMDA-receptor subunits in plasticity.

Novel optical tools for controlling plasticity and unique Photoactivatable Ca2+ probes for targeted imaging

Lecture
Date:
Monday, January 4, 2016
Hour: 14:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Shai Berlin
|
Dept of Molecular and Cell Biology and Helen Wills Neuroscience Institute University of California, Berkeley

: Neuronal plasticity is a unique property that describes the ability of the system to undergo long-lasting changes, typically as a result of experience. This paradigm, initially discovery by Bliss and Lomo and dubbed long term potentiation (LTP), describes a scenario where the post-synaptic responses increase in strength for long durations, following a particular pre-synaptic stimulus. Conversely, LT-Depression, describes the long lasting depression of synaptic responses. Today, these phenomena are commonly used to describe the molecular model for learning and memory. A large body of work has implicated more than a hundred proteins and factors in modulating LTP and LTD, and thereby memory. Unfortunately, there is still a lively debate regarding the true necessity and exact role of each player. The need for new techniques and approaches to further explore synaptic function and dysfunction has never been more pressing, as the number of people developing neurodegenerative diseases rises exponentially to epidemic scales, with the aging population. These diseases are characterized by a strong decline in the number of synapses and in the ability of synapses to undergo plasticity, ultimately resulting in the severe decline of cognitive function- such as learning and memory. To better scrutinize synaptic plasticity and probe the function and role of its initiators (i.e. NMDA receptors and calcium ions), I have developed novel light-gated NMDA receptors and photoactivatable fluorescent Ca2+-probes to monitor synaptic activity with unmet spatio-temporal resolution and reversibility. I use the latter to examine the roles of specific NMDA-receptor subunits in plasticity.

Pages

All events, 2016

Dissecting striatal circuits in learning and decision making

Lecture
Date:
Thursday, January 28, 2016
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Ilana Witten
|
Princeton Neuroscience Institute, NJ

I will describe two lines of work in mice aimed at dissecting the role of neuromodulation in the striatum in regulating reward-related learning and decision making. The first story addresses the question of how dopaminergic neurons that innervate the striatum support both learning and action generation, with results suggesting that distinct subpopulations of dopamine neurons support each function. The second story identifies a role for cholinergic interneurons in the ventral striatum in the formation of reward-context associations, with results pointing to a potent ability of the cholinergic neurons in regulating behaviorally-relevant plasticity.

Sensory mechanisms of long-distance navigation in birds

Lecture
Date:
Sunday, January 17, 2016
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Dmitry Kishkinev
|
Research Fellow, School of Biological Sciences, Queen's University Belfast, Northern Ireland, UK

Displacement studies have clearly showed that birds are able to perform true navigation, i.e. they can find direction leading to destination from unfamiliar territory. Yet, the sensory mechanisms of navigation remain poorly understood. There are two primary hypotheses explaining the sensory nature of navigation: (1) a magnetic map hypothesis proposes that birds use parameters of the geomagnetic field which predictably distributed on the globe. This hypothesis claims that the magnetic receptor cells used for navigation reside in the upper beak (the so-called ‘beak organ’), and transmit information via the trigeminal nerve to the brain; (2) an olfactory map hypothesis assumes that birds can use olfaction and smell their position by taking advantage of odours predictably distributed in the atmosphere. In the last decade, I together with my co-workers have experimentally tested both hypotheses in migratory songbird species by combining sensory manipulations with displacements both in Europe and North America. Specifically, in our main model species, Eurasian reed warblers (Acrocephalus scirpaceus), a long-distance nocturnal migrant, we have found that this species (and maybe other songbird migrants) use geomagnetic cues and the magnetoreceptors embedded in the trigeminal system for geographical positioning. In parallel with our studies, there is a growing support for olfactory long-distance navigation in sea birds and homing pigeons. In my talk, I will overview the challenges of understanding true navigation in birds and present the most important advances in the context of other relevant studies.

Reprogramming in vivo neural circuits by engineering new synaptic connections

Lecture
Date:
Wednesday, January 13, 2016
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Ithai Rabinowitch
|
Fred Hutchinson Cancer Research Center, Seattle USA

Synaptic connections between neurons are a fundamental building block of neural circuits. They determine circuit function, and shape whole animal behavior. In order to understand the causal role of synapses in regulating circuit function I have developed a novel synaptic engineering approach that consists of genetically inserting new electrical synapses between specified neurons in vivo. I have successfully implemented this technique in C. elegans circuits and have used it in a variety of applications. For example, for revealing a coincidence detecting mechanism in a nose-touch circuit, for switching olfactory preferences from attraction to a favorable odor into aversion, and for investigating a cross-modal mechanism that compensates for the loss of one sense by sharpening another. Synaptic engineering is thus a powerful new approach that should be widely applicable to a range of animals, enabling to probe, modify and potentially also repair neural circuits. In the long run interventional techniques such as synaptic engineering could make it possible to “upgrade” the nervous system.

PKA signaling network: Visualizing through Macromolecular Assembly and High Resolution Imaging of the Brain

Lecture
Date:
Tuesday, January 12, 2016
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Ronit Ilouz
|
Dept of Pharmacology, University of California San Diego

cAMP dependent Protein kinase (PKA) plays a critical role in numerous neuronal functions including neuronal excitability, synaptic plasticity, learning and memory. Specificity in PKA signaling is achieved in part by the four functionally non-redundant regulatory (R) subunits. The inactive holoenzyme has a dimeric R subunit bound to two Catalytic (C) subunits. The full-length holoenzyme crystal structures allow me to understand how isoform-specific assembly can create distinct holoenzyme structures that each defines its allosteric regulation. High-resolution large-scale mosaic images provide global views of brain sections and allow identification of subcellular features. Analysis of multiple regions demonstrates that the R isoforms are concentrated within discrete regions and express unique and consistent patterns of subcellular localization. Using the miniSOG technique for correlating fluorescent microscopy with electron microscopy I find RIβ in the mitochondria within the cristae and the inner membrane, and in the nucleus, modifying the existing dogma of cAMP-PKA in the nucleus. Down-regulation of the nuclear RIβ, but not RIIβ, decreased L-LTP related signaling as reported by CREB phosphorylation in primary neuronal cultures, consistent with deficits observed in RIβ knockout mice. Furthermore, we show that a point mutation in the RIβ gene, that is associated with a neurodegenerative disease, abolishes dimerization while retaining robust interaction with the catalytic subunit. As a consequence, the interaction with an A-Kinase Anchoring Protein (AKAP) was also diminished. This mutation abolishes the AKAP-mediated targeting of RIβ holoenzymes to specific cellular compartments, which is consistent with an accumulation of RIβ in neuronal inclusions in patients carrying this mutation. These diverse interdisciplinary tools are defining PKA signaling as highly localized complexes that are targeted to specific sites in the cell in close to proximity to substrates and other signaling molecules where activity is then regulated by local levels of cAMP and calcium as well as kinases and phosphatases.

Representation of motion in hierarchical neural systems

Lecture
Date:
Tuesday, January 5, 2016
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Avner Wallach
|
Faculty of Health Sciences, University of Ottawa, Canada

The vertebrate nervous system evolved a highly complex hierarchical architecture. While considerable progress has been made in describing the representation of behaviorally relevant state-variables by high-level circuits, how these circuits interact with low-level networks and modulate behavior is still poorly understood. In this talk I will describe two studies that begin to address this issue by exploring the transformations of motion representation across different tiers of the neural hierarchy. In the first study, conducted at Ehud Ahissar's lab at the Weizmann Institute of Science, we explored the generation and processing of rhythmic phase coding, previously reported as a key state-variable in cortical processing of rodent vibrissal perception. Using closed-loop motion control in anesthetized rats, we found that the vibrissal mechanoreceptors generate this invariant phase representation, which is then differentially processed by the various secondary brainstem populations. In the second study, underway in Leonard Maler's lab at the University of Ottawa, we focus on the preglomerular complex (PG) of the weakly electric fish Apteronotus leptorhynchus. This small, densely packed diencephalic structure serves as an exclusive gateway from the hindbrain and midbrain circuits to the telencephalon, which is involved in memory formation and spatial navigation. We found both spatial and temporal compression of motion related information conveyed through the PG bottleneck, suggesting an effective 'division of labor' between the low and high levels of the hierarchy.

Novel optical tools for controlling plasticity and unique Photoactivatable Ca2+ probes for targeted imaging

Lecture
Date:
Monday, January 4, 2016
Hour: 14:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Shai Berlin
|
Dept of Molecular & Cell Biology & Helen Wills Neuroscience Institute University of California, Berkeley

Neuronal plasticity is a unique property that describes the ability of the system to undergo long-lasting changes, typically as a result of experience. This paradigm, initially discovery by Bliss and Lomo and dubbed long term potentiation (LTP), describes a scenario where the post-synaptic responses increase in strength for long durations, following a particular pre-synaptic stimulus. Conversely, LT-Depression, describes the long lasting depression of synaptic responses. Today, these phenomena are commonly used to describe the molecular model for learning and memory. A large body of work has implicated more than a hundred proteins and factors in modulating LTP and LTD, and thereby memory. Unfortunately, there is still a lively debate regarding the true necessity and exact role of each player. The need for new techniques and approaches to further explore synaptic function and dysfunction has never been more pressing, as the number of people developing neurodegenerative diseases rises exponentially to epidemic scales, with the aging population. These diseases are characterized by a strong decline in the number of synapses and in the ability of synapses to undergo plasticity, ultimately resulting in the severe decline of cognitive function- such as learning and memory. To better scrutinize synaptic plasticity and probe the function and role of its initiators (i.e. NMDA receptors and calcium ions), I have developed novel light-gated NMDA receptors and photoactivatable fluorescent Ca2+-probes to monitor synaptic activity with unmet spatio-temporal resolution and reversibility. I use the latter to examine the roles of specific NMDA-receptor subunits in plasticity.

Novel optical tools for controlling plasticity and unique Photoactivatable Ca2+ probes for targeted imaging

Lecture
Date:
Monday, January 4, 2016
Hour: 14:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Shai Berlin
|
Dept of Molecular and Cell Biology and Helen Wills Neuroscience Institute University of California, Berkeley

: Neuronal plasticity is a unique property that describes the ability of the system to undergo long-lasting changes, typically as a result of experience. This paradigm, initially discovery by Bliss and Lomo and dubbed long term potentiation (LTP), describes a scenario where the post-synaptic responses increase in strength for long durations, following a particular pre-synaptic stimulus. Conversely, LT-Depression, describes the long lasting depression of synaptic responses. Today, these phenomena are commonly used to describe the molecular model for learning and memory. A large body of work has implicated more than a hundred proteins and factors in modulating LTP and LTD, and thereby memory. Unfortunately, there is still a lively debate regarding the true necessity and exact role of each player. The need for new techniques and approaches to further explore synaptic function and dysfunction has never been more pressing, as the number of people developing neurodegenerative diseases rises exponentially to epidemic scales, with the aging population. These diseases are characterized by a strong decline in the number of synapses and in the ability of synapses to undergo plasticity, ultimately resulting in the severe decline of cognitive function- such as learning and memory. To better scrutinize synaptic plasticity and probe the function and role of its initiators (i.e. NMDA receptors and calcium ions), I have developed novel light-gated NMDA receptors and photoactivatable fluorescent Ca2+-probes to monitor synaptic activity with unmet spatio-temporal resolution and reversibility. I use the latter to examine the roles of specific NMDA-receptor subunits in plasticity.

Pages

All events, 2016

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All events, 2016

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