All events, 2018

Transmission of Memories Across Generations

Lecture
Date:
Wednesday, October 31, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Oded Rechavi
|
Dept of Neurobiology, Wise Faculty of Life Sciences and Sagol School of Neuroscience, Tel Aviv University

In C.elegans nematodes small RNAs enable transmission of epigenetic responses across multiple generations. The mechanism that allows small RNA inheritance in the germline is being elucidated, and multiple factors, which are needed for this type of epigenetic inheritance per se have been identified. Different environmental conditions, including exposure to viruses, starvation, and heat stress generate heritable small RNA responses. It is still unclear whether endogenous small RNAs, similarly to exogenous small RNAs, can move between cells, and from the soma to the germline (breaching the “Weismann barrier, and allowing inheritance). We are interested in the provocative possibility that heritable small RNA responses can alter the progeny’s behavior, by altering the function of the worm’s nervous system. I the seminar I will discuss our recent findings, ideas, and theories.

Convergence of hunger and thirst in the insular cortex

Lecture
Date:
Sunday, October 28, 2018
Hour: 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Yoav Livneh
|
Beth Israel Deaconess Medical Center and Harvard Medical School

Hierarchical dynamics of visual inference

Lecture
Date:
Thursday, October 25, 2018
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Jochen Braun
|
Institute of Biology Otto-von-Guericke Unversity, Magdeburg

Visual input is noisy, variable, and ambiguous. Optimal inference of physical causes is challenging even for a restricted set of causes (e.g., orientations and spatial frequencies). It is well understood (e.g., Veliz-Cuba et al., 2016) that stochastic dynamical systems can approximate optimal inference by continuously accumulating and evaluating visual evidence. I will argue that the dynamics of multi-stable perception is consistent with just such an inference mechanism. Its psychophysically observable characteristics fully constrain a hierarchical dynamics with three levels, the lowest of which may conceivably correspond to cortical columns or clusters of columns. Given suitable inputs, this hierarchical dynamics accumulates and evaluates noisy evidence to make nearly optimal categorical discriminations. Moreover, its dynamical features seem to afford functional benefits in a volatile world, such as balancing stability and sensitivity of inference. References: Cao, Pastukhov, Mattia, Braun (2016) Collective activity of many bistable assemblies reproduces characteristic dynamics of multistable perception. J. Neurosci., 36: 6957-72. Veliz-Cuba, Kilpatrick, Josic (2016) Stochastic models of evidence accumulation in changing environments. SIAM Review, 58: 264-289.

Emotional valence and implicit memory formation under anesthesia: Neural mechanisms in the amygdala and pre-frontal cortex

Lecture
Date:
Wednesday, October 24, 2018
Hour: 14:00 - 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Nir Samuel (PhD Thesis Defense)
|
Rony Paz Lab, Dept of Neurobiology, WIS

Background: The aim of anaesthesia is to eliminate awareness and prevent memory of the various aversive stimuli of medical procedures. Yet in a portion of cases, patients can recall events that occurred during surgery resulting in risks of adverse psychological outcomes. Fear conditioning offers a robust behavioral model to study this phenomenon, while the abundant evidence implicating the amygdala-medial prefrontal cortex (mPFC) circuit in acquisition, consolidation and retrieval of these memories offers a natural hypothesis for the neural mechanisms. Objective: We aimed to study the effect of anaesthesia on stimulus valence, acquisition and memory and to identify the correlates in the mPFC-amygdala circuit using a primate model and clinically relevant doses of anesthesia. Materials and methods: Two non-human primates acquired aversive memories by tone-odor classical conditioning under anesthesia with different doses of ketamine, a non-competitive antagonist of NMDA and midazolam, a GABA agonist. Both agents are in wide clinical use. We simultaneously recorded single neurons in the BLA and mPFC. Analyses focused on behavioral and neural evidence suggesting maintained valence, acquisition and retention of memory. Results: Seventy-six full sessions from two non-human primates entered analysis. We recorded 172 amygdala and 189 dACC neurons respectively. We found evidence of successful aversive conditioning under both anesthetics and in all doses. Under anesthesia, we found behavioral evidence of retention in 46% of sessions matched by a complementary response of 16.2% and 18.7% of amygdala and mPFC neurons respectively. An increased and escalating amygdala and mPFC response during acquisition predicted later retention and correlated the behavioral result. The behavioral and neural representation of aversive valence was sufficient to drive learning and affected conditioning outcome. Conclusion: Our results suggest that under anesthesia, the perception of stimuli and implicit aversive memory formation may be maintained. We show patterns in the amygdala-mPFC circuit that precede and predict this phenomenon and that may serve future monitoring strategies of anesthetized patients. The use of a primate model and therapeutic doses of common anesthetics affecting both GABA and NMDA transmission improves the possible translation of our findings.

Emotional valence and implicit memory formation under anesthesia: Neural mechanisms in the amygdala and pre-frontal cortex

Lecture
Date:
Wednesday, October 24, 2018
Hour: 14:00 - 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Nir Samuel (PhD Thesis Defense)
|
Rony Paz Lab, Dept of Neurobiology, WIS

Background: The aim of anaesthesia is to eliminate awareness and prevent memory of the various aversive stimuli of medical procedures. Yet in a portion of cases, patients can recall events that occurred during surgery resulting in risks of adverse psychological outcomes. Fear conditioning offers a robust behavioral model to study this phenomenon, while the abundant evidence implicating the amygdala-medial prefrontal cortex (mPFC) circuit in acquisition, consolidation and retrieval of these memories offers a natural hypothesis for the neural mechanisms. Objective: We aimed to study the effect of anaesthesia on stimulus valence, acquisition and memory and to identify the correlates in the mPFC-amygdala circuit using a primate model and clinically relevant doses of anesthesia. Materials and methods: Two non-human primates acquired aversive memories by tone-odor classical conditioning under anesthesia with different doses of ketamine, a non-competitive antagonist of NMDA and midazolam, a GABA agonist. Both agents are in wide clinical use. We simultaneously recorded single neurons in the BLA and mPFC. Analyses focused on behavioral and neural evidence suggesting maintained valence, acquisition and retention of memory. Results: Seventy-six full sessions from two non-human primates entered analysis. We recorded 172 amygdala and 189 dACC neurons respectively. We found evidence of successful aversive conditioning under both anesthetics and in all doses. Under anesthesia, we found behavioral evidence of retention in 46% of sessions matched by a complementary response of 16.2% and 18.7% of amygdala and mPFC neurons respectively. An increased and escalating amygdala and mPFC response during acquisition predicted later retention and correlated the behavioral result. The behavioral and neural representation of aversive valence was sufficient to drive learning and affected conditioning outcome. Conclusion: Our results suggest that under anesthesia, the perception of stimuli and implicit aversive memory formation may be maintained. We show patterns in the amygdala-mPFC circuit that precede and predict this phenomenon and that may serve future monitoring strategies of anesthetized patients. The use of a primate model and therapeutic doses of common anesthetics affecting both GABA and NMDA transmission improves the possible translation of our findings.

Synapsins regulate alpha-synuclein function

Lecture
Date:
Tuesday, October 23, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Daniel Gitler
|
Dept of Physiology and Cell Biology/Faculty of Health Sciences and Zlotowksi Center for Neuroscience Ben-Gurion University of the Negev

The normal function of alpha-synuclein, a protein involved in Parkinson's Disease and other synucleinopathies, remains elusive. Though recent studies suggest that alpha-synuclein is a physiological attenuator of synaptic vesicle recycling, mechanisms remain unclear. Our data show that synapsin – a cytosolic protein with established roles in synaptic vesicle mobilization and clustering – is required for alpha-synuclein function. Furthermore, we show that the two proteins interact in a reversible manner in the synapse and that in the absence of synapsins, the localization of alpha-synuclein to synapses is deficient. Our data suggest a model where alpha-synuclein and synapsin cooperate in clustering SVs and attenuating recycling.

Information processing at hippocampal synapses

Lecture
Date:
Thursday, October 18, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. J. Simon Wiegert
|
Center for Molecular Neurobiology Hamburg (ZMNH) University Medical Center Hamburg-Eppendorf

Synapses change their strength in response to specific activity patterns. This functional plasticity is assumed to be the brain’s primary mechanism for information storage. We combine optogenetic and chemogenetic control of synapses in rat hippocampal slice cultures with calcium and glutamate imaging of their spines and boutons. This approach enables us to perform all-optical quantal analysis of synaptic transmission, to induce long-term potentiation (LTP), long-term depression (LTD), or both forms of plasticity in sequence, to chronically manipulate activity and to follow the fate of individual synapses for 7 days. We ask how plasticity and activity are integrated at Schaffer collateral synapses over time. Our findings suggest that activity-dependent changes in the transmission strength of individual synapses are transient, but have long-lasting consequences for synaptic lifetime.

Serotonin and Autism Therapeutics: Insights from Human Mutations and Mouse Models

Lecture
Date:
Sunday, October 14, 2018
Hour: 10:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Randy Blakely
|
Director, Florida Atlantic University New Brain Institute, Florida

Signs of serotonergic dysfunction appeared more than 50 years ago with findings of hyperserotonemia in a subset of subjects with ASD, work replicated in multiple studies across the years, and accompanied by supportive data in human and animal studies. Owing to the early elaboration of serotonergic neurons in the mammalian CNS, and genetic evidence for male-specific linkage to ASD overlying the SERT gene locus, we screened multiplex ASD families for evidence of penetrant coding variants in the serotonin transporter, SERT, reporting these in 2005 and evidence that the most common of these, SERT Ala56, demonstrates alterations in the three core domains of the disorder when introduced into the mouse genome, in 2012. More recently, we have identified signaling pathways that lead to aberrant hyperactivity of SERT Ala56 in vitro and in vivo, leading to a novel therapeutic approach, involving manipulation of p38 MAPK. The talk will review the history of the work and next steps in understanding the serotonergic contribution to ASD features arising from other mutations and environmental perturbations.

"What is it like to be a bat?" - A pathway to the answer from the Integrated Information Theory

Lecture
Date:
Sunday, October 7, 2018
Hour: 12:30 - 13:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Naotsugu Tsuchiya
|
School of Psychological Sciences, Monash Institute of Cognitive & Clinical Neuroscience Monash University, Australia

What does it feel like to be a bat? Is conscious experience of echolocation closer to that of vision or audition? Or, echolocation is non-conscious processing and it doesn't feel anything? This famous question of bats' experience, posed by a philosopher Thomas Nagel in 1974, clarifies the difficult nature of the mind-body problem. Why a particular sense, such as vision, has to feel like vision, but not like audition, is puzzling. This is especially so given that any conscious experience is supported by neuronal activity. Activity of a single neuron appears fairly uniform across modalities, and even similar to those for non-conscious processing. Without any explanation on why a particular sense has to feel as the way it does, researchers even cannot approach the question of the bats' experience. Is there any theory that gives us a hope for such explanation? Currently, probably none, except for one. Integrated Information Theory (IIT), proposed by Tononi in 2004 has a potential to offer a plausible explanation. IIT essentially claims that any system that is composed of causally interacting mechanisms can have conscious experience. And precisely how the system feels like is determined by the way the mechanisms influence each other in a holistic way. In this talk, I will give a brief explanation of the essence of IIT and provide initial empirical partial tests of the theory, proposing a potential scientific pathway to approach bats' conscious experience. If IIT, or its improved or related versions, is validated enough, it will gain credibility to accept its prediction on rough nature of bats' experience. If we can gain a sophisticated insight as to whether bats' experience is closer to vision or audition, it is already a tremendously big step in consciousness science, which is just a first yet critical one, possibly a similar level of the breakthrough in cosmology in precisely estimating the age of the universe. References: 0) talk slide: https://www.slideshare.net/NaoNaotsuguTsuchiya/17-june-20-empirical-test-of-iit-dresden 1) Andrew M. Haun, Masafumi Oizumi, Christopher K. Kovach, Hiroto Kawasaki, Hiroyuki Oya, Matthew A. Howard, Ralph Adolphs, Naotsugu Tsuchiya, (2017, accepted) “Conscious perception as integrated information patterns in human electrocorticography” eNeuro link 2) Tsuchiya “"What is it like to be a bat?" - a pathway to the answer from the Integrated Information Theory ” Philosophy Compass (2017) link 3) Oizumi M, Tsuchiya N, Amari S, “Unified framework for quantifying causality and integrated information in a dynamical system” (2016) PNAS link

Dynamics of social representations in the prefrontal cortex and their alterations in mouse models of autism

Lecture
Date:
Thursday, August 30, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dana Rubi Levy (PhD Thesis Defense)
|
Ofer Yizhar Lab, Dept of Neurobiology, WIS

The prefrontal cortex (PFC) plays an important role in regulating social functions in mammals, and impairments in this region have been linked with social dysfunction in psychiatric disorders. Yet little is known of how the PFC encodes social information and of how social representations may be altered in such disorders. Here, we show that neurons in the medial PFC (mPFC) of freely behaving mice preferentially respond to socially-relevant sensory cues. Population activity patterns in the mPFC differed considerably between social and nonsocial stimuli and underwent experience-dependent refinement. In Cntnap2 knockout mice, a genetic model of autism, both the categorization of sensory stimuli and the refinement of social representations were impaired. Noise levels in spontaneous population activity were higher in Cntnap2 mice, and correlated strongly with the degree to which social representations were disrupted. Our findings elucidate the encoding of social sensory cues in the mPFC, and provide an important link between altered prefrontal dynamics and autism-associated social dysfunction.

Pages

All events, 2018

Transmission of Memories Across Generations

Lecture
Date:
Wednesday, October 31, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Oded Rechavi
|
Dept of Neurobiology, Wise Faculty of Life Sciences and Sagol School of Neuroscience, Tel Aviv University

In C.elegans nematodes small RNAs enable transmission of epigenetic responses across multiple generations. The mechanism that allows small RNA inheritance in the germline is being elucidated, and multiple factors, which are needed for this type of epigenetic inheritance per se have been identified. Different environmental conditions, including exposure to viruses, starvation, and heat stress generate heritable small RNA responses. It is still unclear whether endogenous small RNAs, similarly to exogenous small RNAs, can move between cells, and from the soma to the germline (breaching the “Weismann barrier, and allowing inheritance). We are interested in the provocative possibility that heritable small RNA responses can alter the progeny’s behavior, by altering the function of the worm’s nervous system. I the seminar I will discuss our recent findings, ideas, and theories.

Convergence of hunger and thirst in the insular cortex

Lecture
Date:
Sunday, October 28, 2018
Hour: 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Yoav Livneh
|
Beth Israel Deaconess Medical Center and Harvard Medical School

Hierarchical dynamics of visual inference

Lecture
Date:
Thursday, October 25, 2018
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Jochen Braun
|
Institute of Biology Otto-von-Guericke Unversity, Magdeburg

Visual input is noisy, variable, and ambiguous. Optimal inference of physical causes is challenging even for a restricted set of causes (e.g., orientations and spatial frequencies). It is well understood (e.g., Veliz-Cuba et al., 2016) that stochastic dynamical systems can approximate optimal inference by continuously accumulating and evaluating visual evidence. I will argue that the dynamics of multi-stable perception is consistent with just such an inference mechanism. Its psychophysically observable characteristics fully constrain a hierarchical dynamics with three levels, the lowest of which may conceivably correspond to cortical columns or clusters of columns. Given suitable inputs, this hierarchical dynamics accumulates and evaluates noisy evidence to make nearly optimal categorical discriminations. Moreover, its dynamical features seem to afford functional benefits in a volatile world, such as balancing stability and sensitivity of inference. References: Cao, Pastukhov, Mattia, Braun (2016) Collective activity of many bistable assemblies reproduces characteristic dynamics of multistable perception. J. Neurosci., 36: 6957-72. Veliz-Cuba, Kilpatrick, Josic (2016) Stochastic models of evidence accumulation in changing environments. SIAM Review, 58: 264-289.

Emotional valence and implicit memory formation under anesthesia: Neural mechanisms in the amygdala and pre-frontal cortex

Lecture
Date:
Wednesday, October 24, 2018
Hour: 14:00 - 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Nir Samuel (PhD Thesis Defense)
|
Rony Paz Lab, Dept of Neurobiology, WIS

Background: The aim of anaesthesia is to eliminate awareness and prevent memory of the various aversive stimuli of medical procedures. Yet in a portion of cases, patients can recall events that occurred during surgery resulting in risks of adverse psychological outcomes. Fear conditioning offers a robust behavioral model to study this phenomenon, while the abundant evidence implicating the amygdala-medial prefrontal cortex (mPFC) circuit in acquisition, consolidation and retrieval of these memories offers a natural hypothesis for the neural mechanisms. Objective: We aimed to study the effect of anaesthesia on stimulus valence, acquisition and memory and to identify the correlates in the mPFC-amygdala circuit using a primate model and clinically relevant doses of anesthesia. Materials and methods: Two non-human primates acquired aversive memories by tone-odor classical conditioning under anesthesia with different doses of ketamine, a non-competitive antagonist of NMDA and midazolam, a GABA agonist. Both agents are in wide clinical use. We simultaneously recorded single neurons in the BLA and mPFC. Analyses focused on behavioral and neural evidence suggesting maintained valence, acquisition and retention of memory. Results: Seventy-six full sessions from two non-human primates entered analysis. We recorded 172 amygdala and 189 dACC neurons respectively. We found evidence of successful aversive conditioning under both anesthetics and in all doses. Under anesthesia, we found behavioral evidence of retention in 46% of sessions matched by a complementary response of 16.2% and 18.7% of amygdala and mPFC neurons respectively. An increased and escalating amygdala and mPFC response during acquisition predicted later retention and correlated the behavioral result. The behavioral and neural representation of aversive valence was sufficient to drive learning and affected conditioning outcome. Conclusion: Our results suggest that under anesthesia, the perception of stimuli and implicit aversive memory formation may be maintained. We show patterns in the amygdala-mPFC circuit that precede and predict this phenomenon and that may serve future monitoring strategies of anesthetized patients. The use of a primate model and therapeutic doses of common anesthetics affecting both GABA and NMDA transmission improves the possible translation of our findings.

Emotional valence and implicit memory formation under anesthesia: Neural mechanisms in the amygdala and pre-frontal cortex

Lecture
Date:
Wednesday, October 24, 2018
Hour: 14:00 - 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Nir Samuel (PhD Thesis Defense)
|
Rony Paz Lab, Dept of Neurobiology, WIS

Background: The aim of anaesthesia is to eliminate awareness and prevent memory of the various aversive stimuli of medical procedures. Yet in a portion of cases, patients can recall events that occurred during surgery resulting in risks of adverse psychological outcomes. Fear conditioning offers a robust behavioral model to study this phenomenon, while the abundant evidence implicating the amygdala-medial prefrontal cortex (mPFC) circuit in acquisition, consolidation and retrieval of these memories offers a natural hypothesis for the neural mechanisms. Objective: We aimed to study the effect of anaesthesia on stimulus valence, acquisition and memory and to identify the correlates in the mPFC-amygdala circuit using a primate model and clinically relevant doses of anesthesia. Materials and methods: Two non-human primates acquired aversive memories by tone-odor classical conditioning under anesthesia with different doses of ketamine, a non-competitive antagonist of NMDA and midazolam, a GABA agonist. Both agents are in wide clinical use. We simultaneously recorded single neurons in the BLA and mPFC. Analyses focused on behavioral and neural evidence suggesting maintained valence, acquisition and retention of memory. Results: Seventy-six full sessions from two non-human primates entered analysis. We recorded 172 amygdala and 189 dACC neurons respectively. We found evidence of successful aversive conditioning under both anesthetics and in all doses. Under anesthesia, we found behavioral evidence of retention in 46% of sessions matched by a complementary response of 16.2% and 18.7% of amygdala and mPFC neurons respectively. An increased and escalating amygdala and mPFC response during acquisition predicted later retention and correlated the behavioral result. The behavioral and neural representation of aversive valence was sufficient to drive learning and affected conditioning outcome. Conclusion: Our results suggest that under anesthesia, the perception of stimuli and implicit aversive memory formation may be maintained. We show patterns in the amygdala-mPFC circuit that precede and predict this phenomenon and that may serve future monitoring strategies of anesthetized patients. The use of a primate model and therapeutic doses of common anesthetics affecting both GABA and NMDA transmission improves the possible translation of our findings.

Synapsins regulate alpha-synuclein function

Lecture
Date:
Tuesday, October 23, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Daniel Gitler
|
Dept of Physiology and Cell Biology/Faculty of Health Sciences and Zlotowksi Center for Neuroscience Ben-Gurion University of the Negev

The normal function of alpha-synuclein, a protein involved in Parkinson's Disease and other synucleinopathies, remains elusive. Though recent studies suggest that alpha-synuclein is a physiological attenuator of synaptic vesicle recycling, mechanisms remain unclear. Our data show that synapsin – a cytosolic protein with established roles in synaptic vesicle mobilization and clustering – is required for alpha-synuclein function. Furthermore, we show that the two proteins interact in a reversible manner in the synapse and that in the absence of synapsins, the localization of alpha-synuclein to synapses is deficient. Our data suggest a model where alpha-synuclein and synapsin cooperate in clustering SVs and attenuating recycling.

Information processing at hippocampal synapses

Lecture
Date:
Thursday, October 18, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. J. Simon Wiegert
|
Center for Molecular Neurobiology Hamburg (ZMNH) University Medical Center Hamburg-Eppendorf

Synapses change their strength in response to specific activity patterns. This functional plasticity is assumed to be the brain’s primary mechanism for information storage. We combine optogenetic and chemogenetic control of synapses in rat hippocampal slice cultures with calcium and glutamate imaging of their spines and boutons. This approach enables us to perform all-optical quantal analysis of synaptic transmission, to induce long-term potentiation (LTP), long-term depression (LTD), or both forms of plasticity in sequence, to chronically manipulate activity and to follow the fate of individual synapses for 7 days. We ask how plasticity and activity are integrated at Schaffer collateral synapses over time. Our findings suggest that activity-dependent changes in the transmission strength of individual synapses are transient, but have long-lasting consequences for synaptic lifetime.

Serotonin and Autism Therapeutics: Insights from Human Mutations and Mouse Models

Lecture
Date:
Sunday, October 14, 2018
Hour: 10:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dr. Randy Blakely
|
Director, Florida Atlantic University New Brain Institute, Florida

Signs of serotonergic dysfunction appeared more than 50 years ago with findings of hyperserotonemia in a subset of subjects with ASD, work replicated in multiple studies across the years, and accompanied by supportive data in human and animal studies. Owing to the early elaboration of serotonergic neurons in the mammalian CNS, and genetic evidence for male-specific linkage to ASD overlying the SERT gene locus, we screened multiplex ASD families for evidence of penetrant coding variants in the serotonin transporter, SERT, reporting these in 2005 and evidence that the most common of these, SERT Ala56, demonstrates alterations in the three core domains of the disorder when introduced into the mouse genome, in 2012. More recently, we have identified signaling pathways that lead to aberrant hyperactivity of SERT Ala56 in vitro and in vivo, leading to a novel therapeutic approach, involving manipulation of p38 MAPK. The talk will review the history of the work and next steps in understanding the serotonergic contribution to ASD features arising from other mutations and environmental perturbations.

"What is it like to be a bat?" - A pathway to the answer from the Integrated Information Theory

Lecture
Date:
Sunday, October 7, 2018
Hour: 12:30 - 13:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Naotsugu Tsuchiya
|
School of Psychological Sciences, Monash Institute of Cognitive & Clinical Neuroscience Monash University, Australia

What does it feel like to be a bat? Is conscious experience of echolocation closer to that of vision or audition? Or, echolocation is non-conscious processing and it doesn't feel anything? This famous question of bats' experience, posed by a philosopher Thomas Nagel in 1974, clarifies the difficult nature of the mind-body problem. Why a particular sense, such as vision, has to feel like vision, but not like audition, is puzzling. This is especially so given that any conscious experience is supported by neuronal activity. Activity of a single neuron appears fairly uniform across modalities, and even similar to those for non-conscious processing. Without any explanation on why a particular sense has to feel as the way it does, researchers even cannot approach the question of the bats' experience. Is there any theory that gives us a hope for such explanation? Currently, probably none, except for one. Integrated Information Theory (IIT), proposed by Tononi in 2004 has a potential to offer a plausible explanation. IIT essentially claims that any system that is composed of causally interacting mechanisms can have conscious experience. And precisely how the system feels like is determined by the way the mechanisms influence each other in a holistic way. In this talk, I will give a brief explanation of the essence of IIT and provide initial empirical partial tests of the theory, proposing a potential scientific pathway to approach bats' conscious experience. If IIT, or its improved or related versions, is validated enough, it will gain credibility to accept its prediction on rough nature of bats' experience. If we can gain a sophisticated insight as to whether bats' experience is closer to vision or audition, it is already a tremendously big step in consciousness science, which is just a first yet critical one, possibly a similar level of the breakthrough in cosmology in precisely estimating the age of the universe. References: 0) talk slide: https://www.slideshare.net/NaoNaotsuguTsuchiya/17-june-20-empirical-test-of-iit-dresden 1) Andrew M. Haun, Masafumi Oizumi, Christopher K. Kovach, Hiroto Kawasaki, Hiroyuki Oya, Matthew A. Howard, Ralph Adolphs, Naotsugu Tsuchiya, (2017, accepted) “Conscious perception as integrated information patterns in human electrocorticography” eNeuro link 2) Tsuchiya “"What is it like to be a bat?" - a pathway to the answer from the Integrated Information Theory ” Philosophy Compass (2017) link 3) Oizumi M, Tsuchiya N, Amari S, “Unified framework for quantifying causality and integrated information in a dynamical system” (2016) PNAS link

Dynamics of social representations in the prefrontal cortex and their alterations in mouse models of autism

Lecture
Date:
Thursday, August 30, 2018
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Dana Rubi Levy (PhD Thesis Defense)
|
Ofer Yizhar Lab, Dept of Neurobiology, WIS

The prefrontal cortex (PFC) plays an important role in regulating social functions in mammals, and impairments in this region have been linked with social dysfunction in psychiatric disorders. Yet little is known of how the PFC encodes social information and of how social representations may be altered in such disorders. Here, we show that neurons in the medial PFC (mPFC) of freely behaving mice preferentially respond to socially-relevant sensory cues. Population activity patterns in the mPFC differed considerably between social and nonsocial stimuli and underwent experience-dependent refinement. In Cntnap2 knockout mice, a genetic model of autism, both the categorization of sensory stimuli and the refinement of social representations were impaired. Noise levels in spontaneous population activity were higher in Cntnap2 mice, and correlated strongly with the degree to which social representations were disrupted. Our findings elucidate the encoding of social sensory cues in the mPFC, and provide an important link between altered prefrontal dynamics and autism-associated social dysfunction.

Pages

All events, 2018

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All events, 2018

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