2013
All events, 2013
Exploring neuronal processing of complex tactile scenes in the somatosensory system of the rat
Lecture
Tuesday, June 11, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Exploring neuronal processing of complex tactile scenes in the somatosensory system of the rat
Prof. Daniel Shulz
Director of Research CNRS
Sensory processing, Neuromodulation and Plasticity lab
Unit of Neuroscience, Information and Complexity Gif sur Yvette, France
(Weston Visiting Professor at WIS)
The tactile sensations mediated by the whisker-to-barrel cortex system allow rodents to efficiently detect and discriminate objects and surfaces. The temporal structure of whisker deflections and the temporal correlation between deflections occurring on several whiskers simultaneously vary for different tactile substrates. We hypothesize that tactile discrimination capabilities rely strongly on the ability of the system to encode different levels of inter-whisker correlations.
To test this hypothesis, we generated complex spatio-temporal patterns of whisker deflections during electrophysiological recordings in the barrel cortex, the ventro-posterior medial (VPM) nucleus of the thalamus and the trigeminal ganglion. A piezoelectric-based stimulator featuring 24 independent and fully adjustable whisker actuators was built for this purpose (Jacob et al., 2010).
Using this stimulator in anesthetized rats, we have previously shown that cortical neurons exhibit direction selectivity to the apparent motion of a multivibrissal stimulus (i.e. an emerging property of the global stimulus), uncorrelated to the local direction of individual whiskers (Jacob et al. 2008). Since a certain level of multiwhisker integration has been reported in the VPM, the nucleus relaying tactile information to the barrel cortex, we showed that emergent properties of multiwhisker stimulations are already coded by VPM neurons although to a lesser degree than in cortex (Ego-Stengel et al., 2012).
Finally, we applied a reverse correlation approach to this problem by using Gaussian white noise stimulation on 24 whiskers and progressively varying the level of temporal correlation among them. Based on spike-triggered analysis for various levels of inter-whisker correlation, our recent findings (Estebanez et al., 2012) show that neuronal cortical networks implement coexisting coding schemes to cope with the varying statistics of the tactile sensory world. We propose a simple and comprehensive framework that not only accounts for most of the previous reported phenomenology of multiwhisker interactions but also provides a physiological role for this functional selectivity in terms of local contrast and global motion detection.
“The Young and the Restless” Adult Neurogenesis in the Mouse Olfactory Bulb
Lecture
Tuesday, June 4, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
“The Young and the Restless” Adult Neurogenesis in the Mouse Olfactory Bulb
Prof. Adi Mizrahi
Dept of Neurobiology and the Edmond and Lily Safra Center for Brain Sciences
The Hebrew University of Jerusalem
The mammalian the olfactory bulb (OB) maintains a continuous inflow of new neurons to its circuitry throughout adulthood. The role of these newborn neurons in sensory processing or the bulbs’ function remains completely unknown. We use in vivo imaging and electrophysiology to study the structure and function of these neurons. I will present our studies of the development and plasticity of adult-born interneurons as well as that of their resident counterparts. Specifically we use two-photon imaging of single neurons to probe their morphology and two-photon targeted patch to study their physiology in high spatiotemporal resolution. I will discuss our data showing that newborn neurons mature to become integral elements of the sensory coding machinery during the very early stages of olfactory processing. Furthermore, we argue that our results challenge some basic dogmas in the field of adult neurogenesis.
A Metric Approach to Olfactory Space
Lecture
Tuesday, May 28, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
A Metric Approach to Olfactory Space
Prof. Noam Sobel
Department of Neurobiology, WIS
Olfaction researchers at all levels are ultimately trying to solve the same problem, namely a transform across three spaces: from the physicochemical space of odor molecules, through the brain space of neural activity, and on to the space of odor perception and its ensuing behavioral decisions. To solve these transforms, one has to be able to measure each one of these spaces independently. As each of these three spaces is apparently of very high dimensionality, we applied principal components analysis (PCA) to data in each of these three domains. We observed that the functional dimensionality of these spaces was significantly lower than their apparent dimensionality. Moreover, the key axis (PC1) was correlated across domains. In other words, the key axis of olfactory perception was correlated with the key axis of odorant structure, and both of these were correlated with the key axis of neural activity in the olfactory system across species. These correlations allowed us to construct a modest but significant predictive framework across domains. In other words, we could now look at the structure of a novel molecule, and predict modest but significant aspects of its perception and ensuing neural activity across species. Beyond this predictive framework, our approach has several implications regarding sensory phenomena within a metric space. For example, it implies a point of sensory convergence where all olfactory mixtures should smell the same. We call this point "olfactory white". Our metric approach also implies points (odors) that are at the upper and lower boundaries of this metric space, and should therefore be odorless. We call these points "infra smell" and "ultra smell". In this talk I will consider the implications of this approach, as well as its potential shortcomings, and their possible solutions.
Tranceformation: Hypnosis in Brain and Body
Lecture
Monday, May 27, 2013
Hour: 14:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Tranceformation: Hypnosis in Brain and Body
Prof. David Spiegel
Psychiatry & Behavioral Sciences, Stanford University School of Medicine
Hypnosis was the first Western form of psychotherapy, yet it remains underutilized in part because of insufficient understanding of its neural basis. Hypnosis involves highly focused attention, coupled with dissociation of aspects of awareness, relatively automatic response to social cues, and an enhanced ability to modulate perception. New evidence regarding this sensory processing ability will be presented, including studies employing event-related potentials, PET and fMRI. Our recent resting state fMRI data demonstrate functional connectivity between the executive control and salience networks among high but not low hypnotizable individuals. This hypnotic ability to modulate perception has clear clinical application, especially in pain and anxiety control. Randomized clinical trials that we have conducted demonstrate the efficacy of hypnosis in reducing pain, anxiety, somatic complications, and procedure duration during radiological interventions.
The consolidation of episodic memory:How it starts, does it ever end.
Lecture
Tuesday, May 21, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
The consolidation of episodic memory:How it starts, does it ever end.
Prof. Yadin Dudai
Department of Neurobiology, WIS
The conversion of short- into long-term event memory, termed ‘systems consolidation’, is an intricate process that may take weeks and months to mature. Recent studies combining real-life behavioral paradigms and functional human brain imaging, have unveiled phases in which memory is registered and then transformed from one type of lasting representation to another, and the corresponding brain signatures. The processes and mechanisms uncovered can account not only for changes in the quality of event recollection over time, but also for the emergence of selective and false recollection.
WIS-Australia Symposium on Metabolic Syndroms
Conference
Sunday, May 12, 2013
Hour: 08:00 - 16:45
Location:
The David Lopatie Conference Centre
WIS-Australia Symposium on Metabolic Syndroms
Movement vigor, impulsivity, and the cost of waiting in the human brain
Lecture
Monday, May 6, 2013
Hour: 14:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Movement vigor, impulsivity, and the cost of waiting in the human brain
Prof. Reza Shadmehr
Department of Biomedical Engineering,
Johns Hopkins School of Medicine.
There is consistency in how health people move their eyes, arms, and legs. What is good about this way of moving, and why has our brain settled on this pattern? Here, I focus on the control of eye movements and suggest that the purpose of any movement is to acquire a more rewarding state. I suggest that the way the brain discounts reward in time strongly affects why we move the way that we do. This framework has the potential to explain why disorders that affect processing of reward in the brain, like Parkinson's disease, depression, and Schizophrenia, result in changes in control of movements.
Predictive information and the brain's internal time
Lecture
Tuesday, April 30, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Predictive information and the brain's internal time
Prof. Naftali Tishby
Director, Interdisciplinary Center for Neural Computation The Hebrew University, Jerusalem
Abstract: One of the most intriguing questions in cognitive neuroscience is how our sensation and perception of time is related to the physical (Newtonian) time axis. In this talk I will argue that our sensation of time is scaled non-linearly with the information we have about the relevant past and future. In other words, we scale our internal clock with the number of "bits" of perceptual and actionable information, as determined by our sensory and planning tasks. To this end, I will introduce a Renormalisation Group procedure of the Bellman equation for Partially Observed Markov Decision Processes (POMDP), and argue that such renormalisation (non-linear rescaling of time) can explain the subjective discounting of rewards, and the emergence of hierarchies and reverse hierarchies in perception and planing.
Finally, I will argue that the structure of our natural language reflects the "fixed point" of this renormalisation group - namely, the divergence of our planning and perception horizons.
Emotional memories and stress: from normal physiology to psychopathology
Conference
Thursday, April 25, 2013
Hour:
Location:
The David Lopatie Conference Centre
Small molecules against Alzheimer’s disease (AD) hallmarks and novel therapeutic targets
Lecture
Tuesday, April 23, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Small molecules against Alzheimer’s disease (AD) hallmarks and novel therapeutic targets
Prof. Abraham Fisher
Israel Institute for Biological Research, Ness Ziona
(On sabbatical at the Dept of Neurobiology, Weizmann Institute, Rehovot)
Major failures in AD patients with several low molecular weight (LMW) compounds and certain immunotherapies indicate that the etiology of the disease is still elusive. Therefore future therapies should address all AD hallmarks, regardless of prime etiological culprits. In this lecture several low molecular weight (LMW) compounds and their respective target(s) are critically discussed as potential treatments for AD including, inter alia: cholinergic modulators [cholinesterase inhibitors (AChE-Is), alpha7-nicotinic agonists, M1 muscarinic agonists], alpha-secretase activators, BACE1 inhibitors, gamma-secretase inhibitors or modulators, inhibitors of beta-amyloids (Abeta) aggregation or Abeta-induced neurotoxicity, inhibitors of tau proteins hyperphosphorylation and/or tau proteins aggregation, GSK-3beta inhibitors and sigma-1 receptor (Sig1R) agonists. Comparison among these compounds is made when possible also with M1 muscarinic agonists and a new compound, AF710B. In this context the M1 muscarinic receptor (M1 mAChR) appears to be a pivotal target for treatment of AD, Parkinson's disease (PD) and Lewy body dementia (LBD). Notably the M1 muscarinic agonists AF102B, AF267B, AF292 are effective cognitive enhancers and disease modifiers with a wide safety margin. Thus - i) AF102B decreased CSF Abeta in AD patients (Nitsch et al, Ann Neurol 2000); ii) AF267B rescued cognitive deficits and decreased Abeta42 and tau pathologies in 3xTg-AD mice (Caccamo et al, Neuron, 2006); and iii) AF102B and AF267B decreased brain alpha-synuclein aggregates in transgenic mice overexpressing human alpha-synuclein (Fisher et al., ADPD 2011). However in spite of their potential in disease modification (DM) and cognitive enhancement, M1 agonists (either orthosteric or allosteric) still do not address a prime disease hallmark, e.g. mitochondrial dysfunctions, which can be ameliorated via the molecular chaperone Sig1R. In this context we have designed a novel molecule, AF710B (MW, 357.5) which shows a novel mechanism of action (MoA) of enhancing neuroprotection and cognition via Sig1R activation and M1 muscarinic allosteric modulation, but not resembling Sig1R, M1 muscarinic (allosteric or orthosteric) and dual Sig1R/M1 agonists, respectively. The effects of AF710B at low concentrations in vitro against neurodegeneration, oxidative stress, Abeta, Tau-phosphorylation and GSK-3beta activation translate into down-regulation of the apoptotic protein Bax and mitochondrial dysfunction, up-regulation of anti-apoptotic Bcl2. AF710B has an exceptional pharmacology being an excellent cognitive enhancer in rats (at 1-30 and 10-100mcg/kg, po in trihexyphenidyl- and in MK801-induced passive avoidance impairments, respectively). AF710B is devoid of side effects, having an unprecedented safety margin > 50,000 (po). Furthermore, AF710B mitigated cognitive impairments, reduced Abeta40, Abeta42 levels and tau pathology and inflammation in 3xTg-AD mice AF710B (at 10 mcg/kg, ip/daily for 2 months; Morris water maze). The unique effects of AF710B can be explained by a super-sensitization of M1 mAChR through a hypothetical heteromerization with Sig1R. Conclusions: Only some of the reviewed compounds can bridge treatment of both cognitive impairments with DM. In this context, AF710B is the 1st reported low MW CNS-penetrable mono-therapy that meets comprehensively this challenge. The unmatched potency of AF710B on cognition and on amyloid and tau pathologies, combined with its beneficial effects on inflammation and mitochondrial dysfunctions, indicates extensive therapeutic advantages for AF710B in AD and other protein-aggregation related diseases vs. a plethora of experimental and licensed treatments.
Keywords: M1 muscarinic receptor, M1 agonist, disease modifiers, beta-amyloids, sigma-1 agonist, tau proteins, alpha-synuclein
Pages
2013
All events, 2013
A Metric Approach to Olfactory Space
Lecture
Tuesday, May 28, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
A Metric Approach to Olfactory Space
Prof. Noam Sobel
Department of Neurobiology, WIS
Olfaction researchers at all levels are ultimately trying to solve the same problem, namely a transform across three spaces: from the physicochemical space of odor molecules, through the brain space of neural activity, and on to the space of odor perception and its ensuing behavioral decisions. To solve these transforms, one has to be able to measure each one of these spaces independently. As each of these three spaces is apparently of very high dimensionality, we applied principal components analysis (PCA) to data in each of these three domains. We observed that the functional dimensionality of these spaces was significantly lower than their apparent dimensionality. Moreover, the key axis (PC1) was correlated across domains. In other words, the key axis of olfactory perception was correlated with the key axis of odorant structure, and both of these were correlated with the key axis of neural activity in the olfactory system across species. These correlations allowed us to construct a modest but significant predictive framework across domains. In other words, we could now look at the structure of a novel molecule, and predict modest but significant aspects of its perception and ensuing neural activity across species. Beyond this predictive framework, our approach has several implications regarding sensory phenomena within a metric space. For example, it implies a point of sensory convergence where all olfactory mixtures should smell the same. We call this point "olfactory white". Our metric approach also implies points (odors) that are at the upper and lower boundaries of this metric space, and should therefore be odorless. We call these points "infra smell" and "ultra smell". In this talk I will consider the implications of this approach, as well as its potential shortcomings, and their possible solutions.
Tranceformation: Hypnosis in Brain and Body
Lecture
Monday, May 27, 2013
Hour: 14:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Tranceformation: Hypnosis in Brain and Body
Prof. David Spiegel
Psychiatry & Behavioral Sciences, Stanford University School of Medicine
Hypnosis was the first Western form of psychotherapy, yet it remains underutilized in part because of insufficient understanding of its neural basis. Hypnosis involves highly focused attention, coupled with dissociation of aspects of awareness, relatively automatic response to social cues, and an enhanced ability to modulate perception. New evidence regarding this sensory processing ability will be presented, including studies employing event-related potentials, PET and fMRI. Our recent resting state fMRI data demonstrate functional connectivity between the executive control and salience networks among high but not low hypnotizable individuals. This hypnotic ability to modulate perception has clear clinical application, especially in pain and anxiety control. Randomized clinical trials that we have conducted demonstrate the efficacy of hypnosis in reducing pain, anxiety, somatic complications, and procedure duration during radiological interventions.
The consolidation of episodic memory:How it starts, does it ever end.
Lecture
Tuesday, May 21, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
The consolidation of episodic memory:How it starts, does it ever end.
Prof. Yadin Dudai
Department of Neurobiology, WIS
The conversion of short- into long-term event memory, termed ‘systems consolidation’, is an intricate process that may take weeks and months to mature. Recent studies combining real-life behavioral paradigms and functional human brain imaging, have unveiled phases in which memory is registered and then transformed from one type of lasting representation to another, and the corresponding brain signatures. The processes and mechanisms uncovered can account not only for changes in the quality of event recollection over time, but also for the emergence of selective and false recollection.
Movement vigor, impulsivity, and the cost of waiting in the human brain
Lecture
Monday, May 6, 2013
Hour: 14:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Movement vigor, impulsivity, and the cost of waiting in the human brain
Prof. Reza Shadmehr
Department of Biomedical Engineering,
Johns Hopkins School of Medicine.
There is consistency in how health people move their eyes, arms, and legs. What is good about this way of moving, and why has our brain settled on this pattern? Here, I focus on the control of eye movements and suggest that the purpose of any movement is to acquire a more rewarding state. I suggest that the way the brain discounts reward in time strongly affects why we move the way that we do. This framework has the potential to explain why disorders that affect processing of reward in the brain, like Parkinson's disease, depression, and Schizophrenia, result in changes in control of movements.
Predictive information and the brain's internal time
Lecture
Tuesday, April 30, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Predictive information and the brain's internal time
Prof. Naftali Tishby
Director, Interdisciplinary Center for Neural Computation The Hebrew University, Jerusalem
Abstract: One of the most intriguing questions in cognitive neuroscience is how our sensation and perception of time is related to the physical (Newtonian) time axis. In this talk I will argue that our sensation of time is scaled non-linearly with the information we have about the relevant past and future. In other words, we scale our internal clock with the number of "bits" of perceptual and actionable information, as determined by our sensory and planning tasks. To this end, I will introduce a Renormalisation Group procedure of the Bellman equation for Partially Observed Markov Decision Processes (POMDP), and argue that such renormalisation (non-linear rescaling of time) can explain the subjective discounting of rewards, and the emergence of hierarchies and reverse hierarchies in perception and planing.
Finally, I will argue that the structure of our natural language reflects the "fixed point" of this renormalisation group - namely, the divergence of our planning and perception horizons.
Small molecules against Alzheimer’s disease (AD) hallmarks and novel therapeutic targets
Lecture
Tuesday, April 23, 2013
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Small molecules against Alzheimer’s disease (AD) hallmarks and novel therapeutic targets
Prof. Abraham Fisher
Israel Institute for Biological Research, Ness Ziona
(On sabbatical at the Dept of Neurobiology, Weizmann Institute, Rehovot)
Major failures in AD patients with several low molecular weight (LMW) compounds and certain immunotherapies indicate that the etiology of the disease is still elusive. Therefore future therapies should address all AD hallmarks, regardless of prime etiological culprits. In this lecture several low molecular weight (LMW) compounds and their respective target(s) are critically discussed as potential treatments for AD including, inter alia: cholinergic modulators [cholinesterase inhibitors (AChE-Is), alpha7-nicotinic agonists, M1 muscarinic agonists], alpha-secretase activators, BACE1 inhibitors, gamma-secretase inhibitors or modulators, inhibitors of beta-amyloids (Abeta) aggregation or Abeta-induced neurotoxicity, inhibitors of tau proteins hyperphosphorylation and/or tau proteins aggregation, GSK-3beta inhibitors and sigma-1 receptor (Sig1R) agonists. Comparison among these compounds is made when possible also with M1 muscarinic agonists and a new compound, AF710B. In this context the M1 muscarinic receptor (M1 mAChR) appears to be a pivotal target for treatment of AD, Parkinson's disease (PD) and Lewy body dementia (LBD). Notably the M1 muscarinic agonists AF102B, AF267B, AF292 are effective cognitive enhancers and disease modifiers with a wide safety margin. Thus - i) AF102B decreased CSF Abeta in AD patients (Nitsch et al, Ann Neurol 2000); ii) AF267B rescued cognitive deficits and decreased Abeta42 and tau pathologies in 3xTg-AD mice (Caccamo et al, Neuron, 2006); and iii) AF102B and AF267B decreased brain alpha-synuclein aggregates in transgenic mice overexpressing human alpha-synuclein (Fisher et al., ADPD 2011). However in spite of their potential in disease modification (DM) and cognitive enhancement, M1 agonists (either orthosteric or allosteric) still do not address a prime disease hallmark, e.g. mitochondrial dysfunctions, which can be ameliorated via the molecular chaperone Sig1R. In this context we have designed a novel molecule, AF710B (MW, 357.5) which shows a novel mechanism of action (MoA) of enhancing neuroprotection and cognition via Sig1R activation and M1 muscarinic allosteric modulation, but not resembling Sig1R, M1 muscarinic (allosteric or orthosteric) and dual Sig1R/M1 agonists, respectively. The effects of AF710B at low concentrations in vitro against neurodegeneration, oxidative stress, Abeta, Tau-phosphorylation and GSK-3beta activation translate into down-regulation of the apoptotic protein Bax and mitochondrial dysfunction, up-regulation of anti-apoptotic Bcl2. AF710B has an exceptional pharmacology being an excellent cognitive enhancer in rats (at 1-30 and 10-100mcg/kg, po in trihexyphenidyl- and in MK801-induced passive avoidance impairments, respectively). AF710B is devoid of side effects, having an unprecedented safety margin > 50,000 (po). Furthermore, AF710B mitigated cognitive impairments, reduced Abeta40, Abeta42 levels and tau pathology and inflammation in 3xTg-AD mice AF710B (at 10 mcg/kg, ip/daily for 2 months; Morris water maze). The unique effects of AF710B can be explained by a super-sensitization of M1 mAChR through a hypothetical heteromerization with Sig1R. Conclusions: Only some of the reviewed compounds can bridge treatment of both cognitive impairments with DM. In this context, AF710B is the 1st reported low MW CNS-penetrable mono-therapy that meets comprehensively this challenge. The unmatched potency of AF710B on cognition and on amyloid and tau pathologies, combined with its beneficial effects on inflammation and mitochondrial dysfunctions, indicates extensive therapeutic advantages for AF710B in AD and other protein-aggregation related diseases vs. a plethora of experimental and licensed treatments.
Keywords: M1 muscarinic receptor, M1 agonist, disease modifiers, beta-amyloids, sigma-1 agonist, tau proteins, alpha-synuclein
DOES LIFE EQUAL INFORMATION PROCESSING?
Lecture
Wednesday, April 17, 2013
Hour: 13:00
Location:
The David Lopatie Conference Centre
DOES LIFE EQUAL INFORMATION PROCESSING?
Dr. Yuval Noah Harari
Dept of History,
Hebrew University, Jerusalem
The subject of this talk will be conversion of the “information processing” paradigm into the control paradigm, not only in the life sciences but also in growing parts of the humanities and social sciences. The second part will focus on the implications of this subject to the study of the brain and consciousness. Is the brain an information processing system? And if so, does this imply that consciousness is an information processing system? What do we miss when we try to understand the world through the information processing paradigm?
Localization of Functions in the Human Brain:Combined Neuroimaging, Intracranial EEG, and Electrical Brain Stimulation
Lecture
Tuesday, April 9, 2013
Hour: 16:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Localization of Functions in the Human Brain:Combined Neuroimaging, Intracranial EEG, and Electrical Brain Stimulation
Prof. Josef Parvizi
Neurology and Neurological Sciences, Stanford University
Throughout the history of neuroscience, from the Chinese to the Egyptians and Romans, it was a key problem to find the seat of human experience. Once it was discovered that the brain is the sole proprietor of the human mind, a second flurry of scientific discourse focused on defining the localization of cognitive functions in the vast mantle of the brain. In my talk, after a brief historical overview, I will discuss the notion of localization of function in the brain in light of recent data from intracranial electrophysiological recordings during real life settings and electrical stimulation of the brain in conscious human subjects.
Neuronal signal integration in dendrites and axons of hippocampal neurons
Lecture
Thursday, April 4, 2013
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Neuronal signal integration in dendrites and axons of hippocampal neurons
Prof. Nelson Sprutson
Howard Hughes Medical Institute, Janelia Farm Research Campus,
Ashburn, VA, USA
The hippocampus is made up of a diverse collection of neurons with complex physiological properties. I will describe our efforts to understand the functional diversity of these neurons. Most of our work has focused on principal neurons (pyramidal neurons in CA1 and subiculum), where we have described a role for dendritic excitability in synaptic integration and plasticity, as well as diversity in the structure, function, and plasticity in two distinct types of pyramidal neurons. In addition, I will describe recent work demonstrating the importance of the axon as an integrative structure in some inhibitory interneurons in the hippocampus.
Empathic helping in rats and its modulation by social parameters
Lecture
Tuesday, April 2, 2013
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Empathic helping in rats and its modulation by social parameters
Dr. Inbal Ben-Ami Bartal
Dept of Neurobiology,
University of Chicago
Empathy, the recognition and sharing of affective states between individuals, is an adaptive response with ancient evolutionary roots. The experience of empathy rises from activation of subcortical neural circuits in the brain stem, thalamus and paralimbic areas that are highly conserved across mammalian species. Primarily, it is crucial for the survival of altricial mammals to be able to respond to the needs of offspring appropriately. More broadly, communication of emotions promotes group survival, by alerting against potential threats and, depending on context, inducing pro-social actions. Behavioral homologues of empathy have been observed in different non-human animals. For instance, it has been clearly established that rodents display emotional contagion of others’ distress, and are motivated to alleviate another rat’s distress. We found that rats intentionally released a cagemate trapped in a restrainer, even when social contact was prevented. When a second restrainer containing a highly palatable food (chocolate chips) was present, rats opened both restrainers and typically shared the chocolate. Since only cagemates were tested, it is unclear if these behaviors generalize to strangers. Helping others is costly and resource depleting, and should thus be discriminately extended. In humans, the expression of empathically motivated pro-social behavior is dependent on social context, where people are more motivated to help in-group members than out-group members. Correspondingly, emotional contagion is modulated by familiarity in rodents. Mice have been found to display heightened pain sensitivity when witnessing a cagemate in pain, but not a stranger in pain. To investigate these questions, we are currently exploring the effect of social parameters such as familiarity and relatedness on the expression of empathic helping in rats.
Pages
2013
All events, 2013
There are no events to display