All events, All years

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.

Motor learning with unstable neural representations

Lecture
Date:
Wednesday, January 9, 2008
Hour: 11:30
Location:
Wolfson Building for Biological Research
Dr. Uri Rokhni
|
MIT

It is usually assumed that the brain learns by changing neural circuits that are otherwise stable. However, recent experiments in monkeys show that the neural representation of movement in motor cortex is continually changing even without learning, when practicing a familiar task. We set to investigate the reason for these changes. We analyzed the empirical data and found that the changes are slow and random. We constructed a theoretical model of a cortical network that learns a motor skill by changing synaptic strengths. Our model explains how the network can change its synaptic strengths, and neural activity, without changing the motor behavior. Additionally, our model replicates the observed changes when synaptic learning is assumed highly noisy. We speculate that this noise serves to explore different synaptic configurations during learning.

TRP channels, what are they and why are they important

Lecture
Date:
Tuesday, January 8, 2008
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Baruch Minke
|
Hebrew University, Jeruslaem

TRP channels constitute a large and diverse family of proteins that are expressed in many tissues and cell types. The TRP superfamily is conserved throughout evolution from nematodes to humans. The name TRP is derived from a spontaneously occurring Drosophila mutant lacking TRP that responded to a continuous light with a Transient Receptor Potential (therefore, it was designated TRP by Minke). The Drosophila TRP and TRP-like (TRPL) channels, which are activated by the inositol lipid signaling cascade, were used later on to isolate the first mammalian TRP homologues. TRP channels mediate responses to light, nerve growth factors, pheromones, olfaction, taste, mechanical, temperature, pH, osmolarity, vasorelaxation of blood vessels, metabolic stress and pain. Furthermore, mutations in members of the TRP family are responsible for several diseases. Although a great deal is known today about members of the mammalian TRP channels, the exact physiological function and gating mechanisms of most channels are still elusive. Removal of divalent open channel block by depolarization plays a critical role in learning and memory, which is mediated by the N-methyl-D-aspartate (NMDA) channel. TRP channels also exhibit open channel block, but the physiological mechanism of its removal is still unknown. We found that lipids produced by phospholipase C (PLC) and hypoosmotic solutions remove divalent open channel block from the Drosophila TRPL channels without depolarization. Application of lipids increased single channel current and caused impermeable cation influx. The tarantula peptide GsMTx-4 specifically blocks a range of stretch-activated channels, but not by specific interaction with the channel proteins themselves but rather by modification of the channel-lipid boundary. The GsMTx-4 toxin blocked the lipids effect on TRPL channels. We found remarkable commonality between the effects of lipids on the Drosophila TRPL and the mammalian NMDA channels. We suggest a new lipid-dependent mechanism to alleviate open channel block, which operates under physiological conditions, in synergism with depolarization. The profound effect of lipids modulation allows cross talk between channel activity and lipid-producing pathways. Joint work with Moshe Parnas, Ben Katz & Shaya Lev

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Persistence and Phase Synchronization Properties of Fixational Eye Movements

Lecture
Date:
Sunday, December 16, 2007
Hour: 14:00
Location:
Wolfson Building for Biological Research
Dr. Shay Moshel
|
Minerva Center & Department of Physics Bar Ilan University, Ramat Gan

The biological visual system is extremely complex; the coordination between the neurological system, the ocular muscles, and the photoreceptors of the retina make it possible for the visual system to produce a continues 3D representation of the real world which provides the ability to distinguish between objects in space, track them, and estimate their relative distances and velocities. For such complex abilities, the retinal image should be persistent enough for the brain to evaluate it, but ephemeral enough to permit a high sampling rate and in order to overcome physical limitations on constant exposure of the photoreceptors. In order to provide accurate depth information it is also required that there is a synchronization between the movement of both eyes. These requirementS are addressed by a complex neuromuscular system that produces multitimescale and synchronization behaviors that are not yet fully understood. We investigated the roles of these different time scale behaviors, especially how they are expressed in the different spatial directions (vertical versus horizontal). In addition, in primates with frontally placed eyes, the synchronization properties of fixational eye movements is related to binocular coordination in order to provide stereopsis, and thus this was also investigated. Results show different scaling behavior between horizontal and vertical movements. When the small ballistic movements, i.e., microsaccades, are removed, the scaling behavior in both axis become similar. Our findings suggest that microsaccades enhance the persistence at short time scales mostly in the horizontal component and much less in the vertical component. We here applied also the phase synchronization decay method to study the synchronization between six combinations of binocular fixational eye movement components. We found that only the right and left horizontal are synchronized with each other and the right and left vertical. Furthermore, the vertical components are significantly more synchronized than the horizontal components. These differences may be due to the need for continuously moving the eyes in the horizontal plane, in order to match the stereoscopic image for different viewing distances.

Can economics learn something from measuring time response?

Lecture
Date:
Tuesday, December 11, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Ariel Rubinstein
|
School of Economics, Tel Aviv University & Dept of Economics, New York University

The lecture will use the results about time response (see Rubinstein (2007), http://arielrubinstein.tau.ac.il/papers/78.pdf ) to discuss the potential meaning of the neuroeconomics approach to economics. Before the lecture please respond to the 15min questionnaire posted at: http://gametheory.tau.ac.il/student/poll.asp?group=1391

Trying to make sense of the cerebellum: models and experiments

Lecture
Date:
Tuesday, December 4, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Opher Donchin
|
Department of Biomedical Engineering Ben Gurion University, Beer Sheva

In this talk I will describe a recent controversy that has arisen regarding the intrinsic properties of Purkinje cells and explain the importance of this controversy to our understanding of Cerebellar function. In brief, it has been shown that Purkinje cell membrane potential is bistable, but there remains significant disagreement about whether this bistability has a functional role. In our lab, we addressed the controversy by recording from Purkinje cells in an awake animal and testing to see whether bistability that had been observed in vitro and in anaesthetized animals could also be seen in a behaving animal. Our findings will not settle the controversy, nor settle the question of the Cerebellum's functional role, but they will significantly shift the terms of the debate. We found that all of the predictions we tested confirmed the potential for a functional role for Purkinje cell bistability. This will force a serious re-evaluation of our understanding of Cerebellar circuitry.

The accessory olfactory (vomeronasal) system: a sensory adapted for social interactions

Lecture
Date:
Tuesday, November 20, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Shlomo Wagner
|
Dept of Biology and Dept of Neurobiology and Ethology, Haifa University

Many mammals rely on pheromones to mediate social interactions. Traditionally pheromones were thought to be detected by the accessory olfactory (vomeronasal) system, but recent studies indicated a central role for the main olfactory system in this function. Thus, unraveling the functional difference between these two chemosensory systems is essential for understanding pheromone-mediated social interactions. In this study we show that mitral cells of the accessory olfactory bulb respond to sensory input in a bimodal manner: a transient response is elicited by low level stimulation, whereas strong stimuli evoke sustained firing that lasts for 10-30 s. This is in sharp contrast to the unimodal response of main olfactory bulb mitral cells. We further show that this difference is dictated by distinct membrane properties of the two neuronal populations. We hypothesize that, via its sustained activity, the accessory olfactory system induces a new sensory state in the animal, reflecting its social context.

Clarifying the functional neuro-anatomy of face processing by combining lesion studies and neuroimaging

Lecture
Date:
Tuesday, November 13, 2007
Hour: 14:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Prof. Bruno Rossion
|
University of Louvain, Belgium

Understanding the functional neuro-anatomy of face processing in the human brain is a long-standing goal of Cognitive Neuroscience. Up to the early 90’s, the most important source of knowledge was from lesion studies, i.e. making correlations between the localization of lesions in groups of brain-damaged patients and their face recognition impairments. The influence of the cognitive approach in Neuropsychology, with an emphasis on single-case functional investigations, as well as the advent of neuroimaging studies in the healthy brain, have considerably reduced the importance of lesion studies in clarifying the neuro-anatomical aspects of face processing. In this talk, my goal will be to illustrate how neuroimaging investigations of single-cases of acquired prosopagnosic patients can still greatly increase our knowledge in this field. Neuroimaging studies of the normal brain have shown that the middle fusiform gyrus (‘FFA’) and the inferior occipital gyrus (‘OFA’) are activated by both detection and identification of faces. Among other observations, our studies of the patient PS, a case of prosopagnosia with normal object recognition, show that the right ‘FFA’ can be recruited to detect faces independently of the ‘OFA’ of the same hemisphere (Rossion et al., 2003). However, fMRI-adaptation investigations suggest that both areas are necessary to perform individual discrimination of faces (Schiltz et al., 2006). Recent observations also show that the the same brain area, here the right ‘FFA’, may be impaired at individual face discrimination while performing normal individual object discrimination. This suggests that clusters of neurons coding specifically for different categories in this area (Grill-Spector et al., 2006) can be functionnally independent. Finally, when structurally intact, non-face preferring areas such as the ventral part of the lateral occipital complex (vLOC) may subtend residual individual discrimination of faces following prosopagnosia. Altogether, these studies show that faces are processed through multiple pathways in the human brain, with a subset of these areas responding preferentially to faces being critical for efficient face recognition.

Compulsive Rats and Compulsive Humans

Lecture
Date:
Tuesday, November 13, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Daphna Joel
|
Dept of Psychology, Tel Aviv University

Obsessive-compulsive disorder (OCD) is a psychiatric disorder affecting 1-3% of the population. Although several brain regions have been implicated in the pathophysiology of OCD, including the basal ganglia-thalamo-cortical circuits and the dopaminergic and serotonergic systems, the ways in which these neural systems interact to produce obsessions and compulsions in patients is currently unknown. Moreover, although to date, there are effective pharmacological and behavioral treatments to OCD, many patients do not respond to these treatments. For obvious reasons, the understanding and treatment of diseases such as OCD, must rely heavily on appropriate animal models that closely mimic their behavioral and if possible their neural manifestations. We have recently developed a new rat model of OCD, in which ‘compulsive’ lever-pressing is induced by the attenuation of an external feedback of this behavior. Compulsive lever-pressing is abolished by selective serotonin reuptake inhibitors, but not by anxiolytic antipsychotic, and non-serotonergic antidepressant drugs, in accordance with the differential efficacy of these drugs in alleviating obsessions and compulsions in OCD patients. Compulsive lever-pressing is also sensitive to manipulations of the orbitofrontal cortex and of the dopaminergic and serotonergic systems, in line with different lines of evidence implicating these systems in the pathophysiology of OCD. The model is used to screen new pharmacological agents with anti-compulsive activity; to map brain regions in which high frequency stimulation exerts an anti-compulsive effect; to test the autoimmune hypothesis of OCD; to assess the role of genetic vulnerability in OCD; to unravel the role of female gonadal sex hormones in compulsive behavior; and to uncover the neural mechanisms of OCD

Molecular Mechanisms for the Initiation and Maintenance of Long Term Memory Storage

Lecture
Date:
Tuesday, November 6, 2007
Hour: 15:00
Location:
Dolfi and Lola Ebner Auditorium
Prof. Eric Kandel
|
Prof., Columbia University, NY Sr Investigator, Howard Hughes Medical Institute

Alzheimers disease amyloid plaques: Tombs or time bombs? Lipids induce release of neurotoxic oligomers from inert amyloid fibrils

Lecture
Date:
Tuesday, October 30, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Dr. Inna Kuperstein
|
Center of Human Genetics, Flanders Institute & KU, Leuven, Belgium

Alzheimer's disease (AD) is associated with the aggregation of Amyloid-beta peptide (Aβ). It is more and more believed that neurotoxicity is caused during the Aβ aggregation process, by soluble Aβ oligomers species, and not by the Aβ fibrils themselves that considered as inert end-products of the aggregation process. Nevertheless, stability of Aβ fibrils might be overestimated. We found that inert Aβ fibrils can be reversed to toxic oligomers in the presence of synthetic phospholipids and lipid rafts components as gangliosids, sphingomyelin and cholesterol. Interestingly, the equilibrium is not shifted towards monomeric Aβ but rather towards soluble amyloid oligomers (backward oligomers). Biochemical and biophysical analysis reveals that backward oligomers are very similar to the oligomers found during the classical aggregation process of monomeric Aβ (forward oligomers). Backward oligomers cause synaptic markers loss and immediate neurotoxicity to primary neurons followed by apoptotic cell death. In addition, mice brain icv. injection of backward amyloid oligomers causes Tau phosphorylation, Caspase 3 activation and memory impairment in mouse similarly to forward oligomers. Finally, we observe that release of toxic oligomers and subsequent neurotoxicity may be caused by other disease-associated amyloid peptides as TAU, Prion 1 and synthetic amyloidogenic peptide in the presence of lipids. We propose that lipid-induced fibrils disassembly and release of soluble oligomers is a common generic mechanism of amyloids. An important implication of our work is that amyloid plaques are not inert and should be considered as potential large reservoirs of neurotoxic oligomers that can rapidly be mobilized by lipids. Although lipid metabolism has been implicated in neurodegenerative diseases the precise involvement of lipids in basic toxicity mechanisms in AD is a major question. Our data could help to understand this Aβ and lipid relationship in more detail.

Understanding Exploratory Behavior

Lecture
Date:
Tuesday, October 23, 2007
Hour: 12:15
Location:
Jacob Ziskind Building
Prof. Ilan Golani
|
Dept of Zoology, Tel Aviv University

Unlike the situation in neurophysiology, where the relevant variables are mostly known, it is not clear what is to be measured in the study of behavior; what is a reliable datum? What are the elementary patterns? To highlight the building blocks of movement and their organization we use 4 tools: (i) we study gradients: along the body dimension, in space and in time (in moment-to-moment behavior, ontogeny, and recovery). Gradients provide natural origins of axes for measurement, reveal how building blocks are gradually added on top of each other to form the animal's full repertoire, and unite seemingly disparate behaviors into continua. (ii) We systematically change coordinate systems, to find the ones highlighting invariant features. We use multiple kinematic variables to describe the behavior. They may or may not cluster into discrete patterns. (iii) We study behavior on more than one scale. For example, along the body dimension we use 2 scales that of the path, and that of multi-limb coordination. Finally, (iv) we segment movement using intrinsic geometrical and statistical properties. By using combinations and conjunctions of the elementary building blocks we work our way up from low level to cognition- and motivation-related constructs. In my talk I will describe how these tools are implemented in a bottom-up study of mouse (Mus musculus) and fly (Drosophila melanogaster) exploratory behavior.

Linear and non-linear fluorescence imaging of neuronal activity

Lecture
Date:
Wednesday, September 19, 2007
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Dr. Jonathan Fisher
|
Howard Hughes Medical Institute, The Rockefeller University, New York

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