2014
All events, 2014
Experience-dependent plasticity in amputees
Lecture
Wednesday, December 31, 2014
Hour: 12:30
Location:
Experience-dependent plasticity in amputees
Dr.Tamar Makin
FMRIB Centre, Nuffield Dept of Clinical Neuroscience
University of Oxford
Abstract: Arm amputation provides a powerful model for studying plasticity, as it results in massive input and output loss consequential to losing a hand. Amputation also leads to profound changes in behaviour, driven by individuals’ need to compensate for severe disability (adaptive behaviour). Despite this strong behavioural pressure, research on amputation has been largely restricted to deprivation-driven (and supposedly passive) brain reorganisation, with little regard for the potential interaction between deprivation and behavioural related plasticity. As a consequence, sensory deprivation is widely held to cause maladaptive plasticity, resulting in phantom pain. Using a range of neuroimaging approaches I examine the extent to which experience modulates brain structure and function in amputees and individuals with congenital hand absence. I present evidence to challenge the proposed link between cortical reorganisation and phantom pain, and instead demonstrate preservation of topographic representations of the missing (‘phantom’) hand. I will show that phantom pain is associated with maintained representation of the phantom hand as opposed to brain plasticity, with potential implications on future treatment. Instead I provide new evidence that adaptive behaviour leads to extensive reorganisation, such that the limb engaging in compensation for disability takes over the cortical territory of the missing hand. In amputees, this process of adaptive plasticity occurs well beyond the traditionally conceptualised “critical period”. Finally, I provide new evidence for the relationship between lateralised limb-use patterns and lateralised structural and functional organisation in the resting brain. Based on this evidence, I suggest that plasticity in amputees is experience-dependant, and is not inherently maladaptive.
A novel approach to the study of neurodegenerative diseases:In vivo screening within the mouse CNS identifies modulators of Huntington disease
Lecture
Tuesday, December 30, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
A novel approach to the study of neurodegenerative diseases:In vivo screening within the mouse CNS identifies modulators of Huntington disease
Dr. Reut Shema
The Broad Institute of MIT and Harvard, and The Picower Institute for Learning and Memory, MIT
Understanding the molecular basis of neurodegenerative diseases (NDDs), and how they interact with the aging process, is one of the greatest challenges in neuroscience. As the most common NDDs, including Alzheimer’s, Parkinson’s, and Huntington’s diseases remain essentially without a cure, the search for therapeutic targets becomes imperative. We have developed a novel platform for the study of NDDs, utilizing the disease-relevant cellular populations in their natural environment. For these screens, which we term SLIC (Synthetic Lethal In the Central nervous system), pooled libraries of lentivirus for knock-down, knock-out, or over-expression of all known genes in the genome are injected into the relevant disease regions in the mouse brain, with one barcoded virus infecting one cell. Comparison, by genomic sequencing, of lentiviruses that are retrieved from wild-type animals, but not from disease model littermates, after various times of incubation in the mouse brain, reveals target genes that function as enhancers of toxicity specific to the disease-associated mutation. We have implemented SLIC for the study of Huntington’s disease, which is the most common inherited NDD caused by abnormal CAG expansion in the Huntingtin gene. We identified the age-regulated glutathione peroxidase 6 (Gpx6) as a modulator of mutant huntingtin toxicity, and show that overexpression of Gpx6 can dramatically alleviate both behavioral and molecular phenotypes associated with a mouse model of Huntington’s disease. SLIC can, in principle, be used in the study of any neurodegenerative disease for which a mouse model exists, promising to reveal modulators of neurodegenerative disease in an unbiased fashion, akin to screens in simpler model organisms.
Biological and artificial curiosity:models, behaviors and robots
Lecture
Thursday, December 25, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Biological and artificial curiosity:models, behaviors and robots
Dr. Goren Gordon
Personal Robots Group, Media Lab, MIT
Abstract: Curiosity is one of the major human drives. Can we model curiosity in biological agents? Can we implement these models in artificial systems? What happens when a curious child meets a curious robot? In this talk I present recent work on the study of curiosity. First, studies of curiosity-driven behaviors in humans and rodents are presented, where we show that biological agents attempt to manage their novelty in a structured manner. A model that captures this structure is presented, wherein emergent exploration behaviors are balanced with novelty-based withdrawal-like actions. The model, which has only a few free parameters, reproduce, explain and predict many observed behaviors in mice and rats. A similar model is implemented in curious robots that learn about their own body and people interacting with them, resulting in emergent behaviors that have similar characteristics to infants’ behaviors. Finally, results from a recent study show that children’s curiosity can increase after interacting with a curious social robot. Future work on studies of infants’, children’s and adults’ curiosity-driven behavior as well as the development of autonomous curious robots, concludes the talk.
Intercellular Communications in Sensory Ganglia Involving Neurons and Satellite Glial Cells: Implications for Chronic Pain
Lecture
Tuesday, December 16, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Intercellular Communications in Sensory Ganglia Involving Neurons and Satellite Glial Cells: Implications for Chronic Pain
Prof. Menachem Hanani
Hadassah-Hebrew University Medical Center, Jerusalem
Abstract:
Current information indicates that glial cells participate in most normal and pathological processes of the central nervous system. Although much less is known about satellite glial cells (SGCs) in sensory ganglia, it appears that these cells share many characteristics with their central counterparts. We found that SGCs in sensory ganglia of mice undergo major changes in a variety chronic of pain models such as axotomy, local and systemic inflammations, neuropathy induced by chemotherapeutic drugs, and diabetic neuropathy. These changes include upregulation of the glial marker glial fibrillary acidic protein (GFAP), increased cell coupling by gap junctions, and augmented responses to ATP via P2 receptors.
We also showed that intercellular communications in the ganglia are mediated by calcium waves, which depend on gap junctions and P2 receptors. Our main hypothesis is that augmentation of these two factors leads to increased excitability of sensory neurons and pain. In support of this idea, blocking gap junctions reduced neuronal excitability and pain. We propose that SGCs play a major role in chronic pain and may be a suitable target for pain therapy.
The neuroeconomics of simple choice
Lecture
Tuesday, December 2, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
The neuroeconomics of simple choice
Antonio Rangel
Bing Professor of Neuroscience, Behavioral Biology & Economics
CALTECH
Neuroeconomics studies what are the computations made by the brain in different decision situations, and how are these computations implemented and constraints by the underlying neurobiology. This talk describe recent fMRI, EEG and eye-tracking experiments designed to understand how the brain computes and compares values during simple decisions, like choosing between an apple and an orange.
Hierarchical process-memory:an ecologically plausible model of the interaction between memory and processes
Lecture
Sunday, November 30, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Hierarchical process-memory:an ecologically plausible model of the interaction between memory and processes
Prof. Uri Hasson
Dept of Psychology and the Neuroscience Institute
Princeton University, NJ
Traditional models of memory dissociate memory from processes. Such tendency is rooted in the analogy between computers’ architecture and the brain, which dissociate the central processing units from the memory units. Based on such conceptualization, many empirical studies focus on simple delay periods in which memory has to be actively maintained but not processed and cases in which the integration between past and present information is undesirable. However, such models are not applicable to the majority of real life processes in which the past and present converge continuously in the processes of incoming information. Based on empirical data we outline a new framework for process-memory that resists the tendency to separate memory from process. We argue that cortical areas, ranging from early sensory areas to high order areas, has the capacity to accumulate information over time. Memory is intrinsic to each and any neural circuit, and is essential for its ability to process information. Furthermore, our data suggest that the process-memory timescale increases from early sensory areas to high order areas. Our hypothesis, that each brain area accumulates information over its preferred timescale, suggests that memories of the recent past are not stored in a few localized working memory buffers, but rather are distributed in an organized hierarchical topography throughout the nervous system. The “work of memory” is performed in virtually every neural circuit, and attentional systems modulate this ongoing processing in accordance with rule- or goal-related constraints.
Neural Correlates of Multisensory Plasticity
Lecture
Tuesday, November 25, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Neural Correlates of Multisensory Plasticity
Dr. Adam Zaidel
Gonda Multidisciplinary Brain Research Center
Bar Ilan University
The ability of the brain to processes and adapt multiple sources of information dynamically, underlies its adept capacity for perception, decision making and action. In this talk, I shall present recent findings of multisensory (visual-vestibular) calibration in behaving monkeys and its neural correlate. Two mechanisms of multisensory calibration were found: i) in the absence of external feedback, “unsupervised” calibration reduces cue conflict by shifting the cues towards one another, and ii) “supervised” calibration reduces conflict with external feedback, by shifting the cues together, in the same direction. Strikingly, supervised calibration can cause an initially accurate cue to shift away from feedback, becoming less accurate. A computational model in which supervised and unsupervised calibration work in parallel, where the former only relies on the multisensory percept, but the latter calibrates cues individually, accounts for the observed behavior. Intriguingly, multisensory tuning curves in the ventral intraparietal (VIP) area shift together with behavioral calibration. While unsupervised calibration likely represents an implicit shift in perception, supervised calibration may incorporate higher level, more explicit, control of multisensory processing.
Electron spin changes during general anesthesia in Drosophila
Lecture
Tuesday, October 28, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Electron spin changes during general anesthesia in Drosophila
Dr. Luca Turin
Institute of Theoretical Physics,
Ulm University, Germany
One hundred sixty years after its discovery, the molecular mechanism of general anesthesia remains a notable mystery. A very wide range of agents ranging from the element xenon to steroids can act as general anesthetics on all animals from protozoa to man, suggesting that a basic cellular mechanism is involved. Electron spin resonance measurements show that volatile general anesthetics cause large changes in electron spin content of Drosophila fruit flies and that the spin responses are different in anesthesia-resistant mutants. These observations are consistent with the idea that general anesthetics perturb electron currents in cells. Electronic structure calculations on anesthetic–protein interactions are consistent with this mechanism and account for hitherto unexplained features of general anesthetic pharmacology.
Relapse to drug use: behavioral and neuronal mechanisms
Lecture
Sunday, September 7, 2014
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Relapse to drug use: behavioral and neuronal mechanisms
Prof. Yavin Shaham
Branch Chief, Behavioral Neuroscience Branch, Intramural Research Program, NIDA-NIH
Cholinergic interneurons and state correlates in dorsomedial and dorsolateral striatum
Lecture
Thursday, September 4, 2014
Hour: 14:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Cholinergic interneurons and state correlates in dorsomedial and dorsolateral striatum
Prof. Geoffrey Schoenbaum, MD,PhD
Branch Chief, National Institute on Drug Abuse, NIH
Pages
2014
All events, 2014
Experience-dependent plasticity in amputees
Lecture
Wednesday, December 31, 2014
Hour: 12:30
Location:
Experience-dependent plasticity in amputees
Dr.Tamar Makin
FMRIB Centre, Nuffield Dept of Clinical Neuroscience
University of Oxford
Abstract: Arm amputation provides a powerful model for studying plasticity, as it results in massive input and output loss consequential to losing a hand. Amputation also leads to profound changes in behaviour, driven by individuals’ need to compensate for severe disability (adaptive behaviour). Despite this strong behavioural pressure, research on amputation has been largely restricted to deprivation-driven (and supposedly passive) brain reorganisation, with little regard for the potential interaction between deprivation and behavioural related plasticity. As a consequence, sensory deprivation is widely held to cause maladaptive plasticity, resulting in phantom pain. Using a range of neuroimaging approaches I examine the extent to which experience modulates brain structure and function in amputees and individuals with congenital hand absence. I present evidence to challenge the proposed link between cortical reorganisation and phantom pain, and instead demonstrate preservation of topographic representations of the missing (‘phantom’) hand. I will show that phantom pain is associated with maintained representation of the phantom hand as opposed to brain plasticity, with potential implications on future treatment. Instead I provide new evidence that adaptive behaviour leads to extensive reorganisation, such that the limb engaging in compensation for disability takes over the cortical territory of the missing hand. In amputees, this process of adaptive plasticity occurs well beyond the traditionally conceptualised “critical period”. Finally, I provide new evidence for the relationship between lateralised limb-use patterns and lateralised structural and functional organisation in the resting brain. Based on this evidence, I suggest that plasticity in amputees is experience-dependant, and is not inherently maladaptive.
A novel approach to the study of neurodegenerative diseases:In vivo screening within the mouse CNS identifies modulators of Huntington disease
Lecture
Tuesday, December 30, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
A novel approach to the study of neurodegenerative diseases:In vivo screening within the mouse CNS identifies modulators of Huntington disease
Dr. Reut Shema
The Broad Institute of MIT and Harvard, and The Picower Institute for Learning and Memory, MIT
Understanding the molecular basis of neurodegenerative diseases (NDDs), and how they interact with the aging process, is one of the greatest challenges in neuroscience. As the most common NDDs, including Alzheimer’s, Parkinson’s, and Huntington’s diseases remain essentially without a cure, the search for therapeutic targets becomes imperative. We have developed a novel platform for the study of NDDs, utilizing the disease-relevant cellular populations in their natural environment. For these screens, which we term SLIC (Synthetic Lethal In the Central nervous system), pooled libraries of lentivirus for knock-down, knock-out, or over-expression of all known genes in the genome are injected into the relevant disease regions in the mouse brain, with one barcoded virus infecting one cell. Comparison, by genomic sequencing, of lentiviruses that are retrieved from wild-type animals, but not from disease model littermates, after various times of incubation in the mouse brain, reveals target genes that function as enhancers of toxicity specific to the disease-associated mutation. We have implemented SLIC for the study of Huntington’s disease, which is the most common inherited NDD caused by abnormal CAG expansion in the Huntingtin gene. We identified the age-regulated glutathione peroxidase 6 (Gpx6) as a modulator of mutant huntingtin toxicity, and show that overexpression of Gpx6 can dramatically alleviate both behavioral and molecular phenotypes associated with a mouse model of Huntington’s disease. SLIC can, in principle, be used in the study of any neurodegenerative disease for which a mouse model exists, promising to reveal modulators of neurodegenerative disease in an unbiased fashion, akin to screens in simpler model organisms.
Biological and artificial curiosity:models, behaviors and robots
Lecture
Thursday, December 25, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Biological and artificial curiosity:models, behaviors and robots
Dr. Goren Gordon
Personal Robots Group, Media Lab, MIT
Abstract: Curiosity is one of the major human drives. Can we model curiosity in biological agents? Can we implement these models in artificial systems? What happens when a curious child meets a curious robot? In this talk I present recent work on the study of curiosity. First, studies of curiosity-driven behaviors in humans and rodents are presented, where we show that biological agents attempt to manage their novelty in a structured manner. A model that captures this structure is presented, wherein emergent exploration behaviors are balanced with novelty-based withdrawal-like actions. The model, which has only a few free parameters, reproduce, explain and predict many observed behaviors in mice and rats. A similar model is implemented in curious robots that learn about their own body and people interacting with them, resulting in emergent behaviors that have similar characteristics to infants’ behaviors. Finally, results from a recent study show that children’s curiosity can increase after interacting with a curious social robot. Future work on studies of infants’, children’s and adults’ curiosity-driven behavior as well as the development of autonomous curious robots, concludes the talk.
Intercellular Communications in Sensory Ganglia Involving Neurons and Satellite Glial Cells: Implications for Chronic Pain
Lecture
Tuesday, December 16, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Intercellular Communications in Sensory Ganglia Involving Neurons and Satellite Glial Cells: Implications for Chronic Pain
Prof. Menachem Hanani
Hadassah-Hebrew University Medical Center, Jerusalem
Abstract:
Current information indicates that glial cells participate in most normal and pathological processes of the central nervous system. Although much less is known about satellite glial cells (SGCs) in sensory ganglia, it appears that these cells share many characteristics with their central counterparts. We found that SGCs in sensory ganglia of mice undergo major changes in a variety chronic of pain models such as axotomy, local and systemic inflammations, neuropathy induced by chemotherapeutic drugs, and diabetic neuropathy. These changes include upregulation of the glial marker glial fibrillary acidic protein (GFAP), increased cell coupling by gap junctions, and augmented responses to ATP via P2 receptors.
We also showed that intercellular communications in the ganglia are mediated by calcium waves, which depend on gap junctions and P2 receptors. Our main hypothesis is that augmentation of these two factors leads to increased excitability of sensory neurons and pain. In support of this idea, blocking gap junctions reduced neuronal excitability and pain. We propose that SGCs play a major role in chronic pain and may be a suitable target for pain therapy.
The neuroeconomics of simple choice
Lecture
Tuesday, December 2, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
The neuroeconomics of simple choice
Antonio Rangel
Bing Professor of Neuroscience, Behavioral Biology & Economics
CALTECH
Neuroeconomics studies what are the computations made by the brain in different decision situations, and how are these computations implemented and constraints by the underlying neurobiology. This talk describe recent fMRI, EEG and eye-tracking experiments designed to understand how the brain computes and compares values during simple decisions, like choosing between an apple and an orange.
Hierarchical process-memory:an ecologically plausible model of the interaction between memory and processes
Lecture
Sunday, November 30, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Hierarchical process-memory:an ecologically plausible model of the interaction between memory and processes
Prof. Uri Hasson
Dept of Psychology and the Neuroscience Institute
Princeton University, NJ
Traditional models of memory dissociate memory from processes. Such tendency is rooted in the analogy between computers’ architecture and the brain, which dissociate the central processing units from the memory units. Based on such conceptualization, many empirical studies focus on simple delay periods in which memory has to be actively maintained but not processed and cases in which the integration between past and present information is undesirable. However, such models are not applicable to the majority of real life processes in which the past and present converge continuously in the processes of incoming information. Based on empirical data we outline a new framework for process-memory that resists the tendency to separate memory from process. We argue that cortical areas, ranging from early sensory areas to high order areas, has the capacity to accumulate information over time. Memory is intrinsic to each and any neural circuit, and is essential for its ability to process information. Furthermore, our data suggest that the process-memory timescale increases from early sensory areas to high order areas. Our hypothesis, that each brain area accumulates information over its preferred timescale, suggests that memories of the recent past are not stored in a few localized working memory buffers, but rather are distributed in an organized hierarchical topography throughout the nervous system. The “work of memory” is performed in virtually every neural circuit, and attentional systems modulate this ongoing processing in accordance with rule- or goal-related constraints.
Neural Correlates of Multisensory Plasticity
Lecture
Tuesday, November 25, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Neural Correlates of Multisensory Plasticity
Dr. Adam Zaidel
Gonda Multidisciplinary Brain Research Center
Bar Ilan University
The ability of the brain to processes and adapt multiple sources of information dynamically, underlies its adept capacity for perception, decision making and action. In this talk, I shall present recent findings of multisensory (visual-vestibular) calibration in behaving monkeys and its neural correlate. Two mechanisms of multisensory calibration were found: i) in the absence of external feedback, “unsupervised” calibration reduces cue conflict by shifting the cues towards one another, and ii) “supervised” calibration reduces conflict with external feedback, by shifting the cues together, in the same direction. Strikingly, supervised calibration can cause an initially accurate cue to shift away from feedback, becoming less accurate. A computational model in which supervised and unsupervised calibration work in parallel, where the former only relies on the multisensory percept, but the latter calibrates cues individually, accounts for the observed behavior. Intriguingly, multisensory tuning curves in the ventral intraparietal (VIP) area shift together with behavioral calibration. While unsupervised calibration likely represents an implicit shift in perception, supervised calibration may incorporate higher level, more explicit, control of multisensory processing.
Electron spin changes during general anesthesia in Drosophila
Lecture
Tuesday, October 28, 2014
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Electron spin changes during general anesthesia in Drosophila
Dr. Luca Turin
Institute of Theoretical Physics,
Ulm University, Germany
One hundred sixty years after its discovery, the molecular mechanism of general anesthesia remains a notable mystery. A very wide range of agents ranging from the element xenon to steroids can act as general anesthetics on all animals from protozoa to man, suggesting that a basic cellular mechanism is involved. Electron spin resonance measurements show that volatile general anesthetics cause large changes in electron spin content of Drosophila fruit flies and that the spin responses are different in anesthesia-resistant mutants. These observations are consistent with the idea that general anesthetics perturb electron currents in cells. Electronic structure calculations on anesthetic–protein interactions are consistent with this mechanism and account for hitherto unexplained features of general anesthetic pharmacology.
Relapse to drug use: behavioral and neuronal mechanisms
Lecture
Sunday, September 7, 2014
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Relapse to drug use: behavioral and neuronal mechanisms
Prof. Yavin Shaham
Branch Chief, Behavioral Neuroscience Branch, Intramural Research Program, NIDA-NIH
Cholinergic interneurons and state correlates in dorsomedial and dorsolateral striatum
Lecture
Thursday, September 4, 2014
Hour: 14:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Cholinergic interneurons and state correlates in dorsomedial and dorsolateral striatum
Prof. Geoffrey Schoenbaum, MD,PhD
Branch Chief, National Institute on Drug Abuse, NIH
Pages
2014
All events, 2014
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