Past events | The department of Brain Sciences

All events, All years

Predictive information and the brain's internal time

Lecture

Date:

Tuesday, April 30, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

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

Date:

Tuesday, April 23, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. 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

Date:

Wednesday, April 17, 2013

Hour: 13:00

Location:

The David Lopatie Conference Centre

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

Date:

Tuesday, April 9, 2013

Hour: 16:00

Location:

Nella and Leon Benoziyo Building for Brain Research

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

Date:

Thursday, April 4, 2013

Hour: 12:30

Location:

Nella and Leon Benoziyo Building for Brain Research

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

Date:

Tuesday, April 2, 2013

Hour: 12:30

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

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.

Molecular Mechanisms Underlying Memory Consolidation and its Possible Implications for Alzheimer Disease New Therapy

Lecture

Date:

Tuesday, March 19, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. Kobi Rosenblum

|

Sagol Dept of Neurobiology, University of Haifa

We are interested in understanding how memories are encoded and retained in the brain and use different methods to uncover the basic molecular and cellular mechanisms underlying learning. Following accumulation of basic science research and data, we recently try to find new ways to enhance memory. Very little is known about drugs which can enhance the consolidation phase of memories in the cortex, the brain structure considered to store at least partially, long term memories. We tested the hypothesis that pharmacological and genetic manipulation of translation machinery, known to be involved in the molecular consolidation phase, enhances positive or negative forms of cortical dependent memories. We found that dephosphorylation (Ser51) of eIF2α specifically in the cortex is both correlated and necessary for normal memory consolidation. In order to reduce eIF2α phosphorylation and improve memory consolidation, we pharmacologically or genetically inhibited the different eIF2α kinases expressed in the brain. In addition, we tested the involvement of eIF2α pathway in mice models of aging and sporadic Alzheimer disease and found strong link between the two. Relevant recent publications: 1. Costa-Mattioli M, Gobert D, Stern E, Gamache K, Colina R, Cuello C, Sossin W, Kaufman R, Pelletier J, Rosenblum K, Krnjević K, Lacaille JC, Nader K, Sonenberg N (2007). eIF2 phosphorylation regulates the switch from short to long-term synaptic plasticity and memory. Cell 6;129(1):195-206. http://www.ncbi.nlm.nih.gov/pubmed/17418795 2. ApoE ε4 is associated with eIF2α phosphorylation and impaired learning in young mice (2013). Yifat Segev, Daniel M. Michaelson, Kobi Rosenblum Neurobiology of Aging. http://www.ncbi.nlm.nih.gov/pubmed/22883908 3. Blocking eIF2a kinase – PKR – Enhances Positive and Negative Forms of Cortex-Dependent Taste Memory (2013). Stern Elad, Chinnakkaruppan Adaikkan, David Orit ,Sonenberg Nahum and Rosenblum Kobi. Journal of Neuroscience (in press).

Quantitative MRI: new measurements reveal structure-function relationships in the living human brain

Lecture

Date:

Wednesday, March 13, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Aviv Mezer

|

Dept of Psychology, Stanford University

Understanding human brain structure and function organization in health, disease and development is one of the great challenges for neuroscience. Magnetic resonance imaging (MRI) is the most valuable technique for noninvasive in vivo imaging of human brain. However, the use of MRI is currently limited, due to the lack of theory that links the specific biological structures to the measured signal. In my presentation I will describe a new quantitative MRI (qMRI) method that directly measures two biophysical properties of the human brain tissue: the macromolecular tissue volume and the macromolecular physico-chemical environment. I will discuss how such quantities can be used for 1) individualize diagnostic applications and 2) mapping structure-function relations in cognitive processes such as reading.

Neural circuits for motor exploration and learning

Lecture

Date:

Tuesday, February 26, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. Jesse Goldberg

|

Department of Neurobiology and Behavior Cornell University

Most human motor behaviors, such as speech or a piano concerto, are not innately programmed but are learned through a gradual process of trial and error. Learning requires exploration and the evaluation of subsequent performance. How are these processes implemented in the brain, and how do they go awry in disease? Songbirds provide a powerful model system to address these questions. Before they develop mature songs, young songbirds ‘babble’—producing highly variable vocalizations that underlie a process of trial-and-error. To investigate the neural mechanisms underlying exploration during learning, I recorded and manipulated neural activity in the basal ganglia, thalamus, and motor cortex-like nuclei in singing juvenile birds. Though the thalamus is traditionally considered a relay between the basal ganglia and cortex, I found that the thalamus, and not its inputs from the BG, was required for vocal variability during babbling. Meanwhile, the BG were required for song learning over time. Currently, my lab is pursuing three specific aims to study precisely how the BG support song learning. First, we are combining neural recordings with acoustic biofeedback to understand how neurons encode how ‘good’ (or ‘bad’) the song sounds. Second, we are developing optogenetic techniques to manipulate the activity of specific neuron subtypes in freely moving, singing birds. Finally, we are developing novel technologies to massively expand the number of neurons we can record simultaneously in singing birds. Basal ganglia circuits in songbirds and humans are very similar, and our overarching goal is to discover basic functions in a tractable model system that may ultimately provide insights into BG diseases such as Parkinson’s, Huntington’s and dystonia.

THE ORCHESTRAL BRAIN:HIGH-FIDELITY CODING WITH CORRELATED NEURONS

Lecture

Date:

Sunday, January 27, 2013

Hour: 14:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Rava da Silveira

|

École Normale Supérieure, Paris, France

While single-cell activity may be well correlated with simple aspects of sensory stumuli, rich stimuli or subtly differing stimuli require concomitant coding by several neurons in a population. It is then natural to ask whether the nature of the coding is ‘orchestral’ in that it relies upon correlation and physiological diversity among cells. Positive correlations in the activity of neurons are widely observed in the brain and previous studies stipulate that these are at best marginally favorable, if not detrimental, to the fidelity of population codes, compared to independent codes. Here, we put forth a scenario in which positive correlations can enhance coding performance by astronomical factors. Specifically, the probability of discrimination error can be suppressed by many orders of magnitude. Likewise, the number of stimuli encoded—the capacity—can be enhanced by similarly large factors. These effects do not necessitate unrealistic correlation values and can occur for populations with as little as a few tens of neurons. The scenario relies upon ‘lock-in’ patterns of activity with which correlation relegates the noise in irrelevant modes. We further demonstrate that, quite generically, coding fidelity is enhanced by physiological heterogeneity. Finally, we formulate heuristic arguments as to the plausibility of ‘lock-in’ patterns and possible experimental tests of the theoretical proposal.

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All events, All years

Quantitative MRI: new measurements reveal structure-function relationships in the living human brain

Lecture

Date:

Wednesday, March 13, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Aviv Mezer

|

Dept of Psychology, Stanford University

Understanding human brain structure and function organization in health, disease and development is one of the great challenges for neuroscience. Magnetic resonance imaging (MRI) is the most valuable technique for noninvasive in vivo imaging of human brain. However, the use of MRI is currently limited, due to the lack of theory that links the specific biological structures to the measured signal. In my presentation I will describe a new quantitative MRI (qMRI) method that directly measures two biophysical properties of the human brain tissue: the macromolecular tissue volume and the macromolecular physico-chemical environment. I will discuss how such quantities can be used for 1) individualize diagnostic applications and 2) mapping structure-function relations in cognitive processes such as reading.

Neural circuits for motor exploration and learning

Lecture

Date:

Tuesday, February 26, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. Jesse Goldberg

|

Department of Neurobiology and Behavior Cornell University

Most human motor behaviors, such as speech or a piano concerto, are not innately programmed but are learned through a gradual process of trial and error. Learning requires exploration and the evaluation of subsequent performance. How are these processes implemented in the brain, and how do they go awry in disease? Songbirds provide a powerful model system to address these questions. Before they develop mature songs, young songbirds ‘babble’—producing highly variable vocalizations that underlie a process of trial-and-error. To investigate the neural mechanisms underlying exploration during learning, I recorded and manipulated neural activity in the basal ganglia, thalamus, and motor cortex-like nuclei in singing juvenile birds. Though the thalamus is traditionally considered a relay between the basal ganglia and cortex, I found that the thalamus, and not its inputs from the BG, was required for vocal variability during babbling. Meanwhile, the BG were required for song learning over time. Currently, my lab is pursuing three specific aims to study precisely how the BG support song learning. First, we are combining neural recordings with acoustic biofeedback to understand how neurons encode how ‘good’ (or ‘bad’) the song sounds. Second, we are developing optogenetic techniques to manipulate the activity of specific neuron subtypes in freely moving, singing birds. Finally, we are developing novel technologies to massively expand the number of neurons we can record simultaneously in singing birds. Basal ganglia circuits in songbirds and humans are very similar, and our overarching goal is to discover basic functions in a tractable model system that may ultimately provide insights into BG diseases such as Parkinson’s, Huntington’s and dystonia.

THE ORCHESTRAL BRAIN:HIGH-FIDELITY CODING WITH CORRELATED NEURONS

Lecture

Date:

Sunday, January 27, 2013

Hour: 14:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Rava da Silveira

|

École Normale Supérieure, Paris, France

While single-cell activity may be well correlated with simple aspects of sensory stumuli, rich stimuli or subtly differing stimuli require concomitant coding by several neurons in a population. It is then natural to ask whether the nature of the coding is ‘orchestral’ in that it relies upon correlation and physiological diversity among cells. Positive correlations in the activity of neurons are widely observed in the brain and previous studies stipulate that these are at best marginally favorable, if not detrimental, to the fidelity of population codes, compared to independent codes. Here, we put forth a scenario in which positive correlations can enhance coding performance by astronomical factors. Specifically, the probability of discrimination error can be suppressed by many orders of magnitude. Likewise, the number of stimuli encoded—the capacity—can be enhanced by similarly large factors. These effects do not necessitate unrealistic correlation values and can occur for populations with as little as a few tens of neurons. The scenario relies upon ‘lock-in’ patterns of activity with which correlation relegates the noise in irrelevant modes. We further demonstrate that, quite generically, coding fidelity is enhanced by physiological heterogeneity. Finally, we formulate heuristic arguments as to the plausibility of ‘lock-in’ patterns and possible experimental tests of the theoretical proposal.

Multisensory processes guide 3-D spatial navigation in echolocating bats

Lecture

Date:

Thursday, January 17, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. Cynthia Moss

|

University of Maryland, College Park, MD

Echolocating bats exhibit an extraordinary array of solutions to the challenges of maneuvering in cluttered environments, pursuing evasive prey, taking food from water surfaces, and landing on the ceiling or walls of confined spaces. Moreover, they are equipped with a biological sonar system that permits spatial navigation and target tracking in complete darkness. By actively controlling the directional aim, timing, frequency content, and duration of echolocation signals to “illuminate” the environment, the bat directly influences the acoustic input available to its sonar imaging system. Detailed analyses of the bat’s sonar behavior suggests that the animal’s actions play into a rich 3-D representation of the environment, which then guides motor commands for subsequent call production, head aim and flight control in an adaptive feedback system. Somatosensory signaling of airflow along the wing membrane also contributes to the exquisite flight control of bats. Recent research reveals that microscopically small hairs embedded in the bat wing play a functional role in sensing air flow, which is important to it to carry out rapid and agile aerial maneuvers. Neurons in bat primary somatosensory cortex (S1) respond to directional stimulation of the wing hairs with low-speed air flow, and this response is diminished after removal of the hairs. The directional preference of cortical S1 neurons indicates that the hairs respond strongest to reverse airflow, and might therefore act as stall detectors. Further, depilation of different functional regions of the wing membrane alters flight behavior in obstacle avoidance tasks by reducing aerial maneuverability, as indicated by decreased turning angles. Collectively, these findings suggest that bat aerial navigation engages multisensory processes that guide a suite of adaptive motor behaviors.

History and News in the Human Visual Cortex

Lecture

Date:

Tuesday, January 15, 2013

Hour: 12:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. Rafi Malach

|

Department of Neurobiology, WIS

In the search for unifying principles of human visual cortex function- it will be proposed that human cortical dynamics can be viewed as shifting between two modes. The first is the well-studied active-mode, informing about visual "News"- i.e. the current perceptual state of the observer. These signals are characterized by fast "ignitions" of highly selective neuronal activity. The second, still poorly understood resting- mode is characterized by slow and wide-spread spontaneous fluctuations. It will be hypothesized that these signals inform about the "History"-i.e. the accumulated statistics of prior cortical activations. Examples of these two modes will be shown- derived from single neurons, local field potentials and functional magnetic resonance imaging (fMRI). Preliminary evidence supporting their functional significance will be presented.

Does the orbitofrontal cortex signal value?

Lecture

Date:

Tuesday, January 8, 2013

Hour: 12:45

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. Geoffrey Schoenbaum

|

Cellular Neurobiology Branch Chief, NIDA, NIH

The orbitofrontal cortex is strongly implicated in good (or at least normal) “decision-making”. Key to good decision-making is knowing the general value or "utility" of available options. Over the past decade, highly influential work has reported that the neurons in the orbitofrontal cortex signal this quantity. Yet the orbitofrontal cortex is typically not necessary for apparent value-based behaviors unless those behaviors require value predictions to be derived from access to complex models of the task, and the neural correlates cited above only part of a much richer representation linking the characteristics of specific outcomes (sensory, timing, unique value) that are expected and the events associated with obtaining them. In this workshop, I will review these data to argue that this aspect of encoding in the orbitofrontal cortex is actually what is critical in explaining the role of this area in both behavior and learning, and that any contribution of this area to economic decision-making stems from its unique role in allowing value to be derived (both within and without) from these environmental models.

Cellular and Circuit Changes Underlying Cortical Learning and Pathology

Lecture

Date:

Monday, January 7, 2013

Hour: 14:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Amos Gdalyahu

|

Dept of Neurobiolgy, School of Medicine, UCLA

Sensory perception is shaped by past learning, and is mediated by neuronal circuits in the sensory cortex. However, what are the changes in these neuronal circuits following learning have remained unknown. To reveal the circuit changes, I developed a new associative fear-learning procedure, and using in vivo 2-photon microscopy measured the circuit responses to the associated stimulus following learning. I discovered that associative learning reduces the percentage of neurons responding to the associated stimulus, while the neurons that still respond increase their response strength. These changes are specific to associative learning because non-associative training triggers a very different set of circuit changes. Therefore, associative learning shapes circuit responses in the sensory cortex for more efficient processing of the conditional stimulus, and for higher signal to noise ratio. The research in my laboratory will continue to address fundamental questions at the levels of cortical neurons, circuits, and behavior. Specifically, how cortical circuits store new information, what are the cortical pathologies in mouse models of autism, and - in the long-term - what are the mechanisms of learning flexible behavior.

Neurophenomenology and the aesthetics of space flight

Lecture

Date:

Sunday, January 6, 2013

Hour: 14:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Prof. Shaun Gallagher

|

Dept of Philosophy, University of Memphis

Introduction: Shaun Gallagher is a philosopher whose interests include embodied and social cognition, perception and agency. His research focuses on phenomenology, philosophy of mind, cognitive science, and hermeneutics, especially the topics of embodied cognition and intersubjectivity. He holds the Lillian and Morrie Moss Chair of Excellence in Philosophy at the University of Memphis. He’s the author of several books, including How the Body Shapes the Mind, Hermeneutics and Education, The Inordinance of Time, and most recently Brainstorming (2008), and (with Dan Zahavi), The Phenomenological Mind (2008). He is editor of The Oxford Handbook of the Self (2011).

Epigenetic transgenerational inheritance alters stress responses in a sexually dimorphic manner

Lecture

Date:

Tuesday, January 1, 2013

Hour: 12:30

Location:

Nella and Leon Benoziyo Building for Brain Research

Prof. David Crews

|

Integrative Biology Section, University of Texas, Austin TX

Ancestral environmental exposures to endocrine disrupting chemicals (EDCs) can promote epigenetic transgenerational inheritance and influence all aspects of the life history of descendants. What happens in the life of descendant is also important, and it is well established that proximate life events such as chronic stress during adolescence modify elements of the adult phenotype, including physiological, neural, and behavioral traits. We use a systems biology approach to investigate in rats to explore this interaction of the ancestral modifications carried transgenerationally in the germ line and the proximate modifications involving chronic restraint stress during adolescence. We find that a single exposure to a common-use fungicide (vinclozolin) three generations removed alters the physiology, behavior, metabolic activity, and transcriptome in discrete brain nuclei in descendant males, causing them to respond differently to chronic restraint stress. This alteration of baseline brain maturation promotes a change in neural genomic activity that correlates with changes in physiology and behavior, revealing the interaction of genetics, environment, and epigenetic transgenerational inheritance in the shaping of the adult phenotype. Further, in many of these traits females differ fundamentally from males, indicating that such effects are not general but sex-specific in how descendants of these progenitor individuals perceive and respond to a common challenges (e.g., chronic restraint stress) experienced during their own life history.

Neural Mechanisms Underlying Selective Attention at a Cocktail Party

Lecture

Date:

Sunday, December 30, 2012

Hour: 14:30

Location:

Gerhard M.J. Schmidt Lecture Hall

Dr. Elana Zion Golumbic

|

Columbia University Medical Center, New York

Our ability to selectively attend to a particular conversation amidst competing input streams (e.g. other speakers) epitomized by the ‘Cocktail Party’ problem, is remarkable. How this demanding perceptual feat is achieved from a neural systems perspective remains unclear and controversial. In this talk I will present data from both invasive and non-invasive electrophysiological recordings in humans, investigating the manner in which selective attention governs the brain’s representation of attended and ignored speech streams using a simulated ‘Cocktail Party’ Paradigm. Results indicate that brain activity dynamically tracks speech streams using both low frequency phase and high frequency amplitude fluctuations, and that optimal encoding likely combines the two. In and near low level auditory cortices, attention ‘modulates’ the representation by enhancing cortical tracking of attended speech streams, but ignored speech remains represented. In higher order regions, the representation appears to become more ‘selective’. Furthermore, when to-be-ignored input has a predictable rhythmic structure, there is even evidence for active suppression of responses to these stimuli, making attention more effective. Viewing the facial movements of the speaker movements of a speech further enhances the selectivity of the neural response. Together, these findings are a testament to the proactive and flexible nature of the neural system which dynamically shapes its internal activity according to environmental and contextual demands.