2019
All events, 2019
Time-resolved neural activity and plasticity in behaving rodents using high field MRI
Lecture
Tuesday, February 5, 2019
Hour: 14:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Time-resolved neural activity and plasticity in behaving rodents using high field MRI
Dr. Noam Shemesh
Champalimaud Centre for the Unknown, Lisbon, Portugal
Neuromodulation of dendritic excitability
Lecture
Tuesday, January 29, 2019
Hour: 14:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Neuromodulation of dendritic excitability
Dr. Mickey London
Edmund and Lily Safra Center for Brain Sciences
The Hebrew University of Jerusalem
The excitability of the apical tuft of layer 5 pyramidal neurons is thought to play a crucial role in behavioral performance and synaptic plasticity. We show that the excitability of the apical tuft is sensitive to adrenergic neuromodulation. Using two-photon dendritic Ca2+ imaging and in vivo whole-cell and extracellular recordings in awake mice, we show that application of the a2A-adrenoceptor agonist guanfacine increases the probability of dendritic Ca2+ events in the tuft and lowers the threshold for dendritic Ca2+ spikes. We further show that these effects are likely to be mediated by the dendritic current Ih. Modulation of Ih in a realistic compartmental model controlled both the generation and magnitude of dendritic calcium spikes in the apical tuft. These findings suggest that adrenergic neuromodulation may affect cognitive processes such as sensory integration, attention, and working memory by regulating the sensitivity of layer 5 pyramidal neurons to top-down inputs.
Synaptic tenacity: When everything changes, do things really stay the same?
Lecture
Tuesday, January 22, 2019
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Synaptic tenacity: When everything changes, do things really stay the same?
Prof. Noam Ziv
Rappaport Faculty of Medicine,
Technion, Haifa
Activity-dependent modifications to synaptic connections – synaptic plasticity – is widely believed to represent a fundamental mechanism for altering network function. This belief also implies, however, that synapses, when not driven to change their properties by physiologically relevant stimuli, should retain these properties over time. Otherwise, physiologically relevant modifications would be gradually lost amidst spurious changes and spontaneous drift. We refer to the capacity of synapses to maintain their properties over behaviorally relevant time scales as 'synaptic tenacity'.
The seminar will examine the challenges to synaptic tenacity imposed by the short lifetimes of synaptic molecules, their inherent dynamics and the logistics of replenishing remote synapses with these molecules at appropriate amounts and stoichiometries. It will then examine the effects these processes have on the (in)stability of synaptic properties , on synaptic size configurations and distributions and on the scaling of these distributions. Finally, it will compare the magnitudes of synaptic changes driven by these processes to those of changes driven by deterministic, activity-dependent synaptic plasticity processes.
The development of the human ventral visual stream
Lecture
Sunday, January 13, 2019
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
The development of the human ventral visual stream
Prof. Kalanit Grill-Spector
Dept of Psychology and Neurosciences Institute
Stanford University, CA
A neural circuit signaling and limiting fluid intake
Lecture
Wednesday, January 9, 2019
Hour: 14:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
A neural circuit signaling and limiting fluid intake
Prof. Sung-Yon Kim
Dept of Chemistry, Institute of Molecular Biology and Genetics
Seoul National University
Drinking enough water is commonly recommended for health, but drinking too much water is dangerous. Therefore, animals have evolved sophisticated mechanisms to prevent harmful overhydration: for one thing, excess intake of water rapidly makes us feel nauseated and avoid further drinking. How do neural circuits mediate this phenomenon? To shed light on this question, we first identified a genetically defined subpopulation of neurons in the parabrachial nucleus (PB) that is activated by water intake. Using fiber photometry, we show that these neurons are activated by the ingestion of fluids, but not solids, and the responses are time-locked to the onset and offset of drinking. Extensive sets of recording experiments demonstrate that the detection mechanism for fluid intake is likely mechanosensory, and the fluid intake signals originate from all parts of the upper digestive tract. By manipulating the activity of the PB neurons, we establish that these neurons are both sufficient and necessary for limiting fluid intake, possibly by recruiting the projection to the median preoptic area. Together, our results identify 1) a central circuit node that can signal and limit fluid intake, 2) the detection mechanism for fluid intake in the periphery, and 3) the neural pathways by which the fluid intake signals are transmitted to the central nervous system.
BLOOD AND STRANGERS – THEIR BEHAVIORAL AND NEURAL CONSEQUENCES
Lecture
Wednesday, January 9, 2019
Hour: 10:15
Location:
Nella and Leon Benoziyo Building for Brain Research
BLOOD AND STRANGERS – THEIR BEHAVIORAL AND NEURAL CONSEQUENCES
Dr. Johan N. Lundstrom
Dept. of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden
Monell Chemical Senses Center, Philadelphia, PA, USA
Department of Psychology, University of Pennsylvania, PA, USA
Behavioral and neuroimaging studies have demonstrated that throughout evolution, visual signals that has been associated with threats enjoy automated and prioritized processing. Based on this, we hypothesized an ability to detect threats also via our nose. In this talk, I will provide an overview of findings from our recent project on olfactory threat signals originating from various sources. Our findings demonstrate that, much like other animals, humans are able to extract odor information that alert us about the presence of specific threats and that this information affect both our neural processing of sensory stimuli as well as the perception of the same.
Neuro-Behavioral Constraints on the Acquisition and Generation of Motor Skills
Lecture
Tuesday, January 1, 2019
Hour: 14:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Neuro-Behavioral Constraints on the Acquisition and Generation of Motor Skills
Dr. Maria Korman
EJ Safra Brain Research Center for the Study of Learning Disabilities
University of Haifa
Acquisition of motor skills often involves the concatenation of single movements into sequences. Along the course of learning, sequential performance becomes progressively faster and smoother, presumably by optimization of both motor planning and motor execution. Following its encoding during training, “how-to” memory undergoes consolidation, reflecting transformations in performance and its neurobiological underpinnings over time. This offline post-training memory process is characterized by two phenomena: reduced sensitivity to interference and the emergence of delayed, typically overnight, gains in performance. Successful learning is a result of strict control (gating) over the on-line and off-line stages of the experience-driven changes in the brain’s organization (neural plasticity). Factors, such as the amount of practice, the passage of time and the affordance of sleep and factors specific to the learning environment may selectively affect, – block or accelerate, - the expression of delayed gains in motor performance. These factors interact in a complex, non-linear manner. Developmental and inter-individual differences impose additional constraints on memory processes (e.g., age, chronotype, clinical condition).
High-level reorganization of the movements as a unit following practice was shown to be subserved by optimization of planning and execution of individual movements. Temporal and kinematic analysis of performance demonstrated that only the offline inter-movement interval shortening (co-articulation) is selectively blocked by the interference experience, while velocity and amplitude, comprising movement time, are interference–insensitive. Sleep, including a day-time sleep, reduces the susceptibility of the memory trace to retroactive behavioural interference and also accelerates the expression of delayed gains in performance. Activity in cortico-striatal areas that was disrupted during the day due to interference and accentuated in the absence of a day-time sleep is restored overnight. Additional line of experiments showed that on-line environmental noise during training (vibro-auditory task-irrelevant stimulation) may be an important modulator of memory consolidation; its impact is ambiguous, presumably contingent on baseline arousal levels of the individual.
1. Albouy G., King B. R., Schmidt C., Desseilles M., Dang-Vu T., Balteau E., Phillips C., Degueldre C., Orban P., Benali H., Peigneux P., Luxen A., Karni A., Doyon J., Maquet P., Korman M. 2016 Cerebral Activity Associated with Transient Sleep-Facilitated Reduction in Motor Memory Vulnerability to Interference Scientific Reports 6:34948
2. Friedman J., Korman M. 2016 Offline optimization of the relative timing of movements in a sequence is blocked by behavioral retroactive interference Frontiers in Human Neuroscience, 10:623
3. Korman M., Herling Z., Levy I., Egbarieh N., Engel-Yeger B., Karni A. 2017 Background matters: minor vibratory sensory stimulation during motor skill acquisition selectively reduces off-line memory consolidation. Neurobiology of Learning and Memory 140:27-32
Pages
2019
All events, 2019
Neuromodulation of dendritic excitability
Lecture
Tuesday, January 29, 2019
Hour: 14:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Neuromodulation of dendritic excitability
Dr. Mickey London
Edmund and Lily Safra Center for Brain Sciences
The Hebrew University of Jerusalem
The excitability of the apical tuft of layer 5 pyramidal neurons is thought to play a crucial role in behavioral performance and synaptic plasticity. We show that the excitability of the apical tuft is sensitive to adrenergic neuromodulation. Using two-photon dendritic Ca2+ imaging and in vivo whole-cell and extracellular recordings in awake mice, we show that application of the a2A-adrenoceptor agonist guanfacine increases the probability of dendritic Ca2+ events in the tuft and lowers the threshold for dendritic Ca2+ spikes. We further show that these effects are likely to be mediated by the dendritic current Ih. Modulation of Ih in a realistic compartmental model controlled both the generation and magnitude of dendritic calcium spikes in the apical tuft. These findings suggest that adrenergic neuromodulation may affect cognitive processes such as sensory integration, attention, and working memory by regulating the sensitivity of layer 5 pyramidal neurons to top-down inputs.
Synaptic tenacity: When everything changes, do things really stay the same?
Lecture
Tuesday, January 22, 2019
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Synaptic tenacity: When everything changes, do things really stay the same?
Prof. Noam Ziv
Rappaport Faculty of Medicine,
Technion, Haifa
Activity-dependent modifications to synaptic connections – synaptic plasticity – is widely believed to represent a fundamental mechanism for altering network function. This belief also implies, however, that synapses, when not driven to change their properties by physiologically relevant stimuli, should retain these properties over time. Otherwise, physiologically relevant modifications would be gradually lost amidst spurious changes and spontaneous drift. We refer to the capacity of synapses to maintain their properties over behaviorally relevant time scales as 'synaptic tenacity'.
The seminar will examine the challenges to synaptic tenacity imposed by the short lifetimes of synaptic molecules, their inherent dynamics and the logistics of replenishing remote synapses with these molecules at appropriate amounts and stoichiometries. It will then examine the effects these processes have on the (in)stability of synaptic properties , on synaptic size configurations and distributions and on the scaling of these distributions. Finally, it will compare the magnitudes of synaptic changes driven by these processes to those of changes driven by deterministic, activity-dependent synaptic plasticity processes.
The development of the human ventral visual stream
Lecture
Sunday, January 13, 2019
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
The development of the human ventral visual stream
Prof. Kalanit Grill-Spector
Dept of Psychology and Neurosciences Institute
Stanford University, CA
A neural circuit signaling and limiting fluid intake
Lecture
Wednesday, January 9, 2019
Hour: 14:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
A neural circuit signaling and limiting fluid intake
Prof. Sung-Yon Kim
Dept of Chemistry, Institute of Molecular Biology and Genetics
Seoul National University
Drinking enough water is commonly recommended for health, but drinking too much water is dangerous. Therefore, animals have evolved sophisticated mechanisms to prevent harmful overhydration: for one thing, excess intake of water rapidly makes us feel nauseated and avoid further drinking. How do neural circuits mediate this phenomenon? To shed light on this question, we first identified a genetically defined subpopulation of neurons in the parabrachial nucleus (PB) that is activated by water intake. Using fiber photometry, we show that these neurons are activated by the ingestion of fluids, but not solids, and the responses are time-locked to the onset and offset of drinking. Extensive sets of recording experiments demonstrate that the detection mechanism for fluid intake is likely mechanosensory, and the fluid intake signals originate from all parts of the upper digestive tract. By manipulating the activity of the PB neurons, we establish that these neurons are both sufficient and necessary for limiting fluid intake, possibly by recruiting the projection to the median preoptic area. Together, our results identify 1) a central circuit node that can signal and limit fluid intake, 2) the detection mechanism for fluid intake in the periphery, and 3) the neural pathways by which the fluid intake signals are transmitted to the central nervous system.
BLOOD AND STRANGERS – THEIR BEHAVIORAL AND NEURAL CONSEQUENCES
Lecture
Wednesday, January 9, 2019
Hour: 10:15
Location:
Nella and Leon Benoziyo Building for Brain Research
BLOOD AND STRANGERS – THEIR BEHAVIORAL AND NEURAL CONSEQUENCES
Dr. Johan N. Lundstrom
Dept. of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden
Monell Chemical Senses Center, Philadelphia, PA, USA
Department of Psychology, University of Pennsylvania, PA, USA
Behavioral and neuroimaging studies have demonstrated that throughout evolution, visual signals that has been associated with threats enjoy automated and prioritized processing. Based on this, we hypothesized an ability to detect threats also via our nose. In this talk, I will provide an overview of findings from our recent project on olfactory threat signals originating from various sources. Our findings demonstrate that, much like other animals, humans are able to extract odor information that alert us about the presence of specific threats and that this information affect both our neural processing of sensory stimuli as well as the perception of the same.
Neuro-Behavioral Constraints on the Acquisition and Generation of Motor Skills
Lecture
Tuesday, January 1, 2019
Hour: 14:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Neuro-Behavioral Constraints on the Acquisition and Generation of Motor Skills
Dr. Maria Korman
EJ Safra Brain Research Center for the Study of Learning Disabilities
University of Haifa
Acquisition of motor skills often involves the concatenation of single movements into sequences. Along the course of learning, sequential performance becomes progressively faster and smoother, presumably by optimization of both motor planning and motor execution. Following its encoding during training, “how-to” memory undergoes consolidation, reflecting transformations in performance and its neurobiological underpinnings over time. This offline post-training memory process is characterized by two phenomena: reduced sensitivity to interference and the emergence of delayed, typically overnight, gains in performance. Successful learning is a result of strict control (gating) over the on-line and off-line stages of the experience-driven changes in the brain’s organization (neural plasticity). Factors, such as the amount of practice, the passage of time and the affordance of sleep and factors specific to the learning environment may selectively affect, – block or accelerate, - the expression of delayed gains in motor performance. These factors interact in a complex, non-linear manner. Developmental and inter-individual differences impose additional constraints on memory processes (e.g., age, chronotype, clinical condition).
High-level reorganization of the movements as a unit following practice was shown to be subserved by optimization of planning and execution of individual movements. Temporal and kinematic analysis of performance demonstrated that only the offline inter-movement interval shortening (co-articulation) is selectively blocked by the interference experience, while velocity and amplitude, comprising movement time, are interference–insensitive. Sleep, including a day-time sleep, reduces the susceptibility of the memory trace to retroactive behavioural interference and also accelerates the expression of delayed gains in performance. Activity in cortico-striatal areas that was disrupted during the day due to interference and accentuated in the absence of a day-time sleep is restored overnight. Additional line of experiments showed that on-line environmental noise during training (vibro-auditory task-irrelevant stimulation) may be an important modulator of memory consolidation; its impact is ambiguous, presumably contingent on baseline arousal levels of the individual.
1. Albouy G., King B. R., Schmidt C., Desseilles M., Dang-Vu T., Balteau E., Phillips C., Degueldre C., Orban P., Benali H., Peigneux P., Luxen A., Karni A., Doyon J., Maquet P., Korman M. 2016 Cerebral Activity Associated with Transient Sleep-Facilitated Reduction in Motor Memory Vulnerability to Interference Scientific Reports 6:34948
2. Friedman J., Korman M. 2016 Offline optimization of the relative timing of movements in a sequence is blocked by behavioral retroactive interference Frontiers in Human Neuroscience, 10:623
3. Korman M., Herling Z., Levy I., Egbarieh N., Engel-Yeger B., Karni A. 2017 Background matters: minor vibratory sensory stimulation during motor skill acquisition selectively reduces off-line memory consolidation. Neurobiology of Learning and Memory 140:27-32
Pages
2019
All events, 2019
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