All events, All years

Pain Selective Anesthesia

Lecture
Date:
Tuesday, June 3, 2008
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Alex Binshtok
|
Harvard Medical School, MA

Although pain is a complex entity, understanding the mechanisms of pain will reveal clues for better control. Perception of nociceptive, inflammatory and neuropathic pain - although initiated by distinctive mechanisms - all depend to some degree on generation and transmission of noxious signals by specific sets of primary sensory afferent neurons, nociceptors. Local anesthetics, by blocking voltage-gated sodium channels, prevent the transmission of nociceptive information and therefore block pain. However, since all local anesthetics act non-selectively on all types of axons, they also cause a loss of innocuous sensation, motor paralysis and autonomic block. Thus, approaches that produce only a selective blockade of pain fibers are of great potential clinical importance. In my talk, I will present a novel method to selectively block pain sensation. Using capsaicin to activate the TRPV1 channel, the noxious thermo-sensitive transducer localized specifically to high-threshold nociceptors, we were able to introduce QX-314, a membrane impermeable and therefore clinically ineffective lidocaine derivative, into nociceptors, and thereby blocked their electrical activity. Neurons that did not express TRPV1 were not blocked by the combination of QX-314 and capsaicin. Injection of QX-314 and capsaicin in vivo together but not alone abolished the response to noxious mechanical and thermal stimuli, without any motor or tactile deficit. This approach could be used clinically to produce long lasting regional analgesia while preserving motor and autonomic function. In addition to applications for dental procedures, surgery and childbirth, this technique could also be used to diminish postoperative and cancer pain, as well as inflammatory and neuropathic pain. Moreover, using TRP channels as a “natural” drug delivery system will enable specific cationic drugs to be targeted only to those cells that express the TRP channel. This technique offers a new strategy for treating pain.

Signal processing in neuronal networks: new vistas for calcium and noise

Lecture
Date:
Monday, June 2, 2008
Hour: 14:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Vladislav Volman
|
The Salk Institute

How neurons and neuronal networks perform signal processing tasks is one of the most important questions in neuroscience. Earlier research had focused on the integrative properties of individual neurons, and the role of activity-dependent inter-neuronal coupling remained obscure. We study the contribution of synaptic short-term plasticity to the detection, amplification, and storage of weak sensory stimuli in local neuronal circuits. Networks with fast plastic coupling show behavior consistent with stochastic resonance. Addition of slow asynchronous coupling mode leads to the qualitatively different properties of signal detection. Networks with asynchronous coupling also are able to hold information about the stimulus seconds after its cessation, thus representing a testable model of working memory, that is supported by experiments. Our results suggest a new, constructive, role in information processing for calcium-sustained synaptic “noise”.

Generation of dopamine neurons from embryonic stem cells for transplantation in Parkinson's disease

Lecture
Date:
Wednesday, May 28, 2008
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof Anders Bjorklund
|
Lund University, Sweden

Fetal mesencephalic tissue has been used as a source of dopaminergic neurons for transplantation in clinical trials with Parkinson’s disease patients and in animal models of Parkinson’s disease. Due to the poor availability of human fetal tissue, and the ethical concerns associated with the use tissue from aborted fetuses, further development of the cell replacement therapy will critically depend on the access to alternative sources of cells for transplantation, based on the use of stem cells as a source of dopaminergic neurons. The recent discovery of Lmx1a and Msx1 as key determinant genes of mesencephalic dopaminergic neuron fate during development (Andersson et al. 2006) has opened new possibilities to drive undifferentiated stem cells towards fully functional mesencephalic dopaminergic neurons. Overexpression of these genes in stable embryonic stem (ES) cell lines is sufficient to generate neurons with almost 100% efficiency into a fully differentiated mesencephalic dopaminergic phenotype. The in vivo data obtained so far indicate that mesencephalic dopaminergic neurons can be generated in large numbers using this approach, and that they survive very well after transplantation to the striatum of 6-hydroxydopamine lesioned rats. In vivo, the Lmx1a- and Msx1-expressing cells develop into fully mature mesencephalic dopaminergic neurons, of both the A9 and A10 subtypes, and grow efficiently to form an extensive TH-positive axonal terminal network throughout the entire host striatum. Using this approach transplantable neurons with what appear to be a complete mesencephalic dopaminergic phenotype can be generated in large numbers from ES cell cultures.

Specialized mechanisms for face processing in the human brain

Lecture
Date:
Tuesday, May 27, 2008
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Galit Yovel
|
Tel Aviv University

It is well established that faces are processed by specialized mechanisms. I will first review evidence for the existence of face-specific processing mechanisms from cognitive studies, functional MRI and electrophysiology (Event-related potentials). These methods provide complementary information about the way information is processed in the brain. It is therefore important to determine whether they all reflect the same mechanism. Our data show that face-selective fMRI markers are strongly associated with cognitive markers of face-selective mechanisms. Furthermore, a simultaneous fMRI-ERP study reveals strong associations between face-selective fMRI regions and event-related potentials. Based on these findings, I will propose an integrated theory on how, where and when faces are represented at early stages of visual processing.

Does urocotin 1 matter?

Lecture
Date:
Monday, May 26, 2008
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Tamas Kozicz
|
Dept of Cellular Animal Physiology Radboud University Nijmegen, The Netherlands

Interactions within the neurovascular unit underlying diseases of the cerebral cortex: evidence from human and animal studies

Lecture
Date:
Tuesday, May 20, 2008
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Alon Friedman
|
Ben Gurion University of the Negev

The Embryonic Neural Crest, from Specification to the Generation of Cellular Movement

Lecture
Date:
Tuesday, May 13, 2008
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Chaya Kalcheim
|
Hebrew University of Jerusalem

The neural crest (NC) is a transient group of progenitors present in vertebrate embryos. Its component cells yield an extensive variety of derivatives such as melanocytes, neurons of many kinds, glial , ectomesenchymal and endocrine cells. Initially, presumptive NC cells are an integral part of the neuroepithelium. Subsequently, a time and axial level-specific conversion from an epithelial to a mesenchymal (EMT) state causes the cells to become motile and engage in migration. Mesenchymal NC cells then advance through stereotyped pathways, reach their homing sites and then differentiate. The molecular network underlying NC delamination and the generation of cell movement remained incompletely understood. We found that a balance between BMP and its inhibitor noggin underlies the emigration of NC independently of earlier cell specification. BMP induces delamination by triggering Wnt1 transcription. Canonical Wnt signaling promotes G1/S transition which is a necessary step for delamination of trunk NC. Successful delamination also requires the activity of effector genes that act on re-organisation of the actin cytoskeleton and alterations in adhesive properties. In this context, we found that both N-cadherin and RhoGTPase signaling play a negative modulatory role on the process. During the course of our work, we observed that in the trunk, NC cells continuously delaminate from the NT for over two days, raising the fundamental question of the source and mechanisms accounting for the production of successive waves of NC progenitors. We found that the first NC to delaminate reside in the dorsal midline of the NT and generate sympathetic ganglia, and successive waves translocate ventrodorsally in the NT to replenish the dorsal midline and then delaminate. Hence, the dorsal midline is a dynamic region traversed sequentially by progenitors that colonize NC derivatives in a ventral to dorsal order (chromaffin cells, sympathetic ganglia, then Schwann cells, DRG and finally melanocytes). Based on our data invoking a dynamic behavior of premigratory NC cells, we hypothesize the existence of a spatiotemporal fate map of derivatives present already within the NT and defined by a specific molecular code.

Plasticity in the circadian clock and social organization in bees

Lecture
Date:
Tuesday, May 6, 2008
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Guy Bloch
|
Hebrew University of Jerusalem

In honeybees (Apis mellifera) natural plasticity in circadian rhythms is associated with the division of labor that organizes their colonies. "Nurse" bees (typically < 2 weeks old) care for brood around-the-clock whereas bees older than 3 weeks of age typically forage for flowers with strong circadian rhythms. We found that nurses care for brood around-the-clock even under a light/dark illumination regime. Brain oscillations in the abundance of the putative clock genes Period and Cryptochrom-m were attenuated or totally suppressed in nurses as compared to foragers, irrespective of the illumination regime. However, nurses showed circadian rhythms in locomotor activity and molecular oscillations in brain clock gene expression shortly after transfer from the hive to constant laboratory conditions. The onset of their activity occurred at the subjective morning, suggesting that some clock components were entrained even while in the hive and active around-the-clock. These results suggest that the hive environment induces reorganization of the molecular clockwork. To test this hypothesis, we studied activity and brain clock gene expression in young bees that were confined to a broodless area on the honeycomb in a light/ dark illuminated observation hive. These bees experienced the hive environment and could interact with other bees, but not with the brood. By contrast to same-age nurses from these colonies, the confined bees showed molecular oscillations in clock gene expression and were more active during the day. These findings are consistent with the hypothesis that interactions with the brood modulate plasticity in the molecular clockwork of the honeybee. These findings together with our previous research, suggest the evolution of sociality shaped the bee clock in a way that facilitate integration of individuals into a complex society.

Rational therapeutic strategies for modifying Alzheimer's disease: Abeta oligomers as the validated target

Lecture
Date:
Monday, April 28, 2008
Hour: 11:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Colin Masters
|
A Laureate Professor in the University of Melbourne & Executive Director of Mental Health Research Institute of Victoria

Medication Development for Treating Addiction: A New Strategy Focusing on the Brain's Dopamine D3 Receptor

Lecture
Date:
Sunday, April 27, 2008
Hour: 10:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Eliot Gardner
|
Chief, Neuropsychopharmacology Section National Institute on Drug Abuse, NIH

Medication discovery and development for the treatment of addictive diseases has focused for many decades on so-called 'substitution' therapies such as methadone for opiate addiction and the nicotine patch or nicotine chewing gum for nicotine addiction. Recent developments in understanding the underlying neurobiology of addiction, craving, and relapse now augur to revolutionize such medication discovery and development. It has long been understood that the meso-accumbens dopamine circuitry of the ventral mesolimbic midbrain and forebrain plays a crucial role in the acutely euphoric 'high' or 'rush' or 'blast' produced by addictive drugs. More recently, it has come to be understood that this brain circuitry is also critically involved in mediating drug craving and relapse to drug-seeking behavior. The dopamine D3 receptor is a remarkable neurotransmitter receptor in the brain. It exists virtually only in those dopaminergic circuits known to mediate drug-induced reward, drug craving, and relapse to drug-seeking behavior. Moreover, blockade of the D3 receptor enhances dopaminergic tone in those circuits. If drug addiction is - to some degree &#8211; a 'reward deficiency' disease, as postulated by many workers in addiction medicine, enhancing dopaminergic tone in these circuits could be therapeutic. This lecture will focus on a lengthy series of experiments- using animal models of addiction - that suggest that highly-selective dopamine D3 receptor antagonists show remarkable therapeutic potential as anti-addiction, anti-craving, and anti-relapse medications."

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Where but not what: The fusion of reafferent and exafferent inputs to perceive the location of objects

Lecture
Date:
Sunday, February 17, 2008
Hour: 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. David Kleinfeld
|
UCSD

Sensory perception in natural environments involves the dual challenge to encode external stimuli and manage the influence of changes in body position that alter the sensory field. To examine mechanisms used to integrate sensory signals elicited by both external stimuli and motor activity, we use a mixture of psychophysics and electrophysiology to study rats trained to perform an active sensory task with a single vibrissa. We identify a nonlinear interaction between vibrissa touch and a motion-derived signal that dynamically labels each neuron with a preferred phase. The observed response enables the rodent to estimate object position in a head-centered reference frame. More generally, our result delineates a computation that is likely to occur in all active sensorimotor systems.

A hierarchy of temporal receptive windows in human cortex

Lecture
Date:
Tuesday, February 12, 2008
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Uri Hasson
|
New York University

Real-world events unfold at different time scales, and therefore cognitive and neuronal processes must likewise occur at different time scales. In the talk I will present a novel procedure that identifies brain regions responsive to the preceding sequence of events (past time) over different time scales. The fMRI activity was measured while observers viewed silent films presented forward, backward, or piecewise-scrambled in time. The results demonstrate that responses in different brain areas are affected by information that has been accumulated over different time scales, with a hierarchy of temporal receptive windows spanning from short (~4 s) to intermediate (~12 s) and long (~ 36 s). Thus, although we adopted an open-ended experimental protocol (free viewing of complex stimuli), we found that parametric manipulation of the temporal structure of a complex movie sequence produced lawful changes in cortical activity across different brain regions. In addition to the reliable cortical response patterns, I will also show that films exerted considerable control over the subjects' behavior (i.e., eye movements or galvanic skin responses). Finally, I will present few applications of this method for studying the neuronal correlates of complex human behaviors under more natural settings.

Information-theoretic analysis of neural data: why do it, why it is challenging, and what can be learned

Lecture
Date:
Tuesday, February 5, 2008
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Jonathan Victor
|
Cornell University

Entropy and information are quantities of interest to neuroscientists, because of their mathematical properties and because they place limits on the performance of a neural system. However, estimating these quantities from neural spike trains is much more challenging than estimating other statistics, such as mean and variance. The central difficulty in estimating information is tightly linked to the properties of information that make it a desirable quantity to estimate. To surmount this fundamental difficulty, most approaches to estimation of information rely (perhaps implicitly) on a model for how spike trains are related. But the nature of these model assumptions vary widely. As a result, information estimates are useful not only in situations in which several approaches provide mutually consistent results, but also in situations in which they differ. These ideas are illustrated with examples from the visual and gustatory systems.

Consequences of the uncertainty principle of measurement for perception and action

Lecture
Date:
Wednesday, January 30, 2008
Hour: 13:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Sergei Gepshtein
|
Brain Science Institute, RIKEN, Japan The Salk Institute for Biological Studies, USA

What can we learn from the octopus about the evolution of neural system for learning and memory?

Lecture
Date:
Tuesday, January 29, 2008
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Binyamin Hochner
|
Hebrew University, Jerusalem

The octopus is an active hunter, a remarkable invertebrate whose complex behaviors rely on exceptionally good visual and tactile senses coupled with highly advanced learning and memory (LM) abilities. Studying the octopus LM system may therefore reveal characteristics universally important for mediation of complex behaviors. We developed slice and isolated brain preparations of the LM area in the octopus brain to characterize the short- and long-term neural plasticity. The importance of these processes for LM are been tested in behavioral experiments. The results support the importance of LTP in behavioral LM and suggest new ideas regarding the organization of short- and long-term memory systems.

Decoding neural signals for the control of movement

Lecture
Date:
Tuesday, January 22, 2008
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Sara Solla
|
Northwestern University

The activity of neurons in primary motor cortex provides the signals that control our ability to execute movements. One of the crucial questions, still unresolved, is that of identifying the coordinate system used in the execution of movements: is it an Euclidean representation of the external space, or an actuator representation of the state of the muscles? We address this question through the analysis of data obtained for an awake behaving monkey. The data includes simultaneous recording of the activity of about one hundred neurons in motor cortex and of the activity of about ten muscles in the relevant limb. The analysis of this data involves a variety of techniques, from linear regression models to nonlinear methods for dimensionality reduction. I will review the current level of achievement in this active area of research and discuss its implications, both for understanding aspects of neural information processing that relate to natural behaviors and for extracting from these neural signals the information needed to guide prosthetic limbs and other types of external devices.

Cortical Maps, Dyanamic Innformation Processing and Perception

Lecture
Date:
Monday, January 21, 2008
Hour: 13:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Christopher Moore
|
McGovern Institute for Brain Research, MIT

I am interested in how neural dynamics, changes in neural sensitivity on the time scale of milliseconds to seconds, support rapid changes in perceptual capability. Our key focus is in testing the hypothesis that dynamics in early sensory cortices, such as the primary somatosensory cortex, play a key role in perception. To examine these issues in a model where detailed invasive studies are possible, we study the vibrissa sensory system of rodents. To examine the broader relevance of these findings, we have a smaller parallel effort I human perception and imaging. A variety of our studies suggest that. In this seminar, I will describe work we have done to understand the 'natural scene' of vibrissa perception, the signals that are generated during active surface contact. I will then describe how these signals are encoded in 2 recently discovered cortical maps, a frequency map, shaped by the resonance properties of the vibrissae, and a direction map, encoding the angle of vibrissa motion. I will then discuss why having these cortical feature columns, with adjacent neurons sharing similar computational processing, may enhance information processing. Specifically, I will argue that this arrangement facilitates dynamic regulation of neural sensitivity by neuromodulators that have a more course spatial precision, on the order of 300-1000 microns. I will briefly mention the hemo-neural hypothesis, the proposal that changes in blood flow and volume may be one source of neural regulation on this spatial scale. I will then describe an example of the dynamic regulation of spatial activation across a cortical map, resulting from adaptation during robust thalamocortical input at 5-25 Hz. I will argue that this adaptation leads to a transition into a state that is enhanced for discrimination of alternative stimuli, but impoverished for detection of novel stimuli (decreased sensitivity). To test the hypothesis that these kinds of cortical dynamics in the primary somatosensory cortex regulate perception, I will describe human MEG experiments showing that changes in the amplitude of SI activation regulate detection probability, and showing that these changes in perception and cortical amplitude are predicted by ongoing rhythmic activity in human SI at 5-25 Hz (the 'mu' rhythm).

Neural Circuits Underlying Sexually Dimorphic Social and Reproductive Behaviors

Lecture
Date:
Wednesday, January 16, 2008
Hour: 12:00
Location:
Dolfi and Lola Ebner Auditorium
Prof. Tali Kimchi
|
Department of Molecular and Cellular Biology Harvard University

My long term interest lies in the mechanistic understanding of sensory processes underlying behavioral responses in laboratory as well as natural wild environments. External sensory cues control complex behaviors such as mating, predator avoidance or orientation in space that are essential for the animal survival and the propagation of the species. In rodents, pheromones play a major role in controlling innate social and sexual responses including mating, nursing and aggression. However, although these behaviors display striking sexual dimorphisms, surprisingly few anatomical and molecular features have been identified that differentiate the male from the female brain. Using genetic and behavioral tools, I have shown that the vomeronasal organ (VNO), an olfactory sensory organ in the nasal cavity of many mammals which detects pheromones, is responsible for the control of male- and female-specific social and sexual behaviors. Amazingly, female mice in which the VNO has been genetically or surgically inactivated engage in male-typical courtship and sexual behaviors including mounting, pelvic thrusting and courtship vocalization, that are indistinguishable from that of normal male mice. These findings suggest a model in which male and female circuits that regulate innate reproductive behaviors exist in the brain of both sexes, while a sex-specific chemosensory network enables pheromonal cues to control the sex-specificity of behavior. To gain a deeper understanding of the molecular and neuronal processes underling sex-specific innate behaviors my lab will combine molecular and genetic tools, together with unique behavioral approaches, to study animal behavioral responses under natural ethologically relevant conditions. Furthermore, to uncover novel VNO-mediated pheromone responses that might have degenerated or been suppressed in inbred laboratory mouse lines, wild-caught mouse strains will be studied in wide range of behavioral, genetically and physiological assays.

Who's Afraid of Chaotic Networks? Model of Sensory and Motor Processing in the Face of Spontaneous Neuronal Activity

Lecture
Date:
Tuesday, January 15, 2008
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Larry Abbott
|
Columbia University

Large, strongly coupled neural networks tend to produce chaotic spontaneous activity. This might appear to make them unsuitable for generating reliable sensory responses or repeatable motor patterns. However, this is not the case. Inputs can induce a phase transition, leading to responses uncontaminated by chaotic "noise". Likewise, appropriately trained feedback units can control the chaos, resulting in a wide variety of repeatable output patterns. These issues will be discussed accompanied by examples and demonstrations.

Beyond Hebbian Plasticity – A Dynamic View of Memory Processing

Lecture
Date:
Monday, January 14, 2008
Hour: 13:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Karim Nader
|
Psychology Dept, McGill University, Montreal

Memory scientists have been inspired and directed for decades in their search for brain mechanisms mediating learning and memory by the postulates of D.O. Hebb. Two of Hebb's most influential postulates include that co-incident activation of pre-and post-synaptic cells could be a mechanism for learning (Hebbian/associative long term potentiation). In addition once a memory is aquired, it initially exists in a fragile, labile state, after which it becomes stabilized/consolidated in the brain. While these postulates have been incredibly influential and largely correct, the data suggests it is may be time to move beyond these postulates. Data will be presented to demonstrate that synapses may not be sensitive to co-incidence of pre- and post-synaptic activation, rather they may be sensitive to probability of their co-activation. Second, we demonstrate that even old consolidated memories return to a labile state when they are remember, and must be reconsolidated in order to persist. This suggests that the traditional Consolidation Hypotheses, including Hebb's postulates, are no longer sufficient to explain the data.

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