All events, All years

Measuring Behavior and Physiology: Bridging the Genotype Phenotype Gap

Conference
Date:
Thursday, March 3, 2011
Hour: 08:00 - 16:30
Location:
Dolfi and Lola Ebner Auditorium

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Stimulus-specific adaptation – beyond the oddball paradigm

Lecture
Date:
Tuesday, March 1, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Prof. Israel Nelken
|
Dept of Neurobiology Hebrew University of Jerusalem

Stimulus-specific adaptation is the decrease in the responses to a common stimulus that does not generalize, or generalize only partially, to other stimuli. Stimulus-specific adaptation in the auditory modality has been studied mostly with oddball sequences, which consist of a common and a rare stimuli. Recently, we started to use a number of other sound sequences in order to study the properties of adaptation in auditory cortex. I will show that (1) SSA is not only the result of the adaptation of the response to the common stimulus - in addition, the responses to the rare tones have a component due to the deviance of the rare tone relative to the regularity set by the common tone; (2) neuronal responses in auditory cortex of rats show sensitivity to finer types of statistical regularities; and (3) SSA can be evoked by other sounds as well, including sounds as similar to each other as two tokens of white noise. These results suggest the existence of a highly sensitive 'statistical machine' that analyzes and interprets the auditory scene.

Deletion of the mouse genomic interval corresponding to human 16p11.2 causes autism-like phenotypes

Lecture
Date:
Wednesday, February 23, 2011
Hour: 15:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Guy Horev
|
Postdoctoral Fellow Cold Spring Harbor Laboratory

Autism is a neuro-cognitive disorder characterized by a broad spectrum of clinical features including repetitive behaviors, restricted interests, language impairment, and altered social interactions. Although chromosome rearrangements affecting specific genomic intervals have been found in patients with autism, the basis for this syndrome is unknown. Deletion of 16p11.2 has been associated with autism, and patients with this deletion have a wide range of clinical symptoms. Here we used chromosome engineering to generate mice with deletion of the 27 genes corresponding to those affected in autism patients with 16p11.2 deletion, as well as mice harboring duplication of the same region. Mice with decreased dosage of this region have unique phenotypes including neonatal lethality, alterations in the volumes of specific brain regions, as well as behaviors reminiscent of clinical features of autism. In particular, mice with 16p11.2 deletion showed behaviors that were repetitive and restricted to specific locations, in contrast to diploid controls that showed a gradual increase in freedom of movement under similar conditions. These findings provide the first functional evidence that compromised dosage of 16p11.2 is causal in autism.

Pavlovian-like behavior in microbes

Lecture
Date:
Tuesday, February 22, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Prof. Yitzhak (Tzachi) Pilpel
|
Department of Molecular Genetics, WIS

The ability to anticipate and prepare in advance to changes in the environment is ascribed to neuronal systems in multi-cellular organisms. Yet by means of gene expression regulatory connectivity microbes too may have evolved to "anticipate" and prepare in advance. I will present evidence for microbial Pavlovian-like conditioning and discuss the similarities and differences to conditioning in the neuronal-cognitive context.

Mechanisms of vocal learning in the songbird: A hypothesis for the role of cortical-basal ganglia circuits

Lecture
Date:
Monday, February 21, 2011
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Michale Fee
|
Dept of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA

Young songbirds, like humans, learn their vocalizations by imitating their parents. This process happens in a series of stages. After memorizing the song of an adult tutor, young birds begin to babble, singing highly random variable sounds. By listening to their own sounds and comparing them with the memory of the tutor song, they gradually refine their song until it can be a nearly exact copy of the tutor. How all this happens at the level of neural circuitry is not yet clear, but recent experiments have begun to shed light on the brain regions and mechanisms involved in the generation of babbling and exploratory variability, in the evaluation of the song, and in the implementation of corrective plastic changes in the motor circuitry. I will describe our current hypothesis for how interacting cortical-basal ganglia circuits implement these various processes underlying vocal learning.

Unraveling the structure of time in the brain

Lecture
Date:
Sunday, February 20, 2011
Hour: 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Michale Fee
|
Dept of Brain and Cognitive Sciences, Massachusetts Institute of Technology, Cambridge, MA

Whether we are speaking, swimming, or playing the piano, we are crucially dependent on our brain?s capacity to step through sequences of neural states. Songbirds provide a marvelous animal model in which to study this phenomenon. Their stereotyped vocalizations have hierarchical temporal structure spanning two orders or magnitude in timescale ? from individual vocal gestures lasting ten milliseconds, to song syllables (~100 msec), to song motifs (~1 sec). Several brain areas have been proposed to control timing at these different timescales. By manipulating these circuits with temperature change and observing the effect on song structure, we have been able to localize a single ?clock? circuit in the premotor vocal pathway. Intracellular neuronal recordings during singing elucidate the mechanism by which this clock circuit operates. Our findings are consistent with the predictions of a synfire-chain model? a synaptically connected chain of neurons in HVC. Our findings are inconsistent with models in which subthreshold dynamics, such as ramps or oscillations, play a role in the control of timing.

A sensorimotor account of phenomenal consciousness

Lecture
Date:
Wednesday, February 16, 2011
Hour: 11:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. J Kevin O'Regan
|
Laboratoire Psychologie de la Perception CNRS - Université Paris Descartes

The problem of consciousness is sometimes divided into two parts: An "easy" part, which involves explaining how one can become aware of of something in the sense of being able to make use of it in one's rational behavior. This is called access consciousness. And a "hard" part, which involves explaining why sensations feel like something, or have a kind of sensory presence, rather than having no feel at all. This is called phenomenal consciousness. Phenomenal consciousness is considered hard because there seems logically no way physical mechanisms in the brain could explain such facts. For example why does red look red, rather than looking green, or rather than sounding like a bell. Indeed why does red have a feel at all? Why do pains hurt instead of just provoking avoidance reactions? The sensorimotor approach provides a way of answering these questions by appealing to the idea that feels like red and pain should not be considered as things that happen to us, but rather as modes of ineraction with the environment. I shall show how the idea can be applied to color, touch, pain, and sensory substitution. In addition to helping understand human consciousness, the approach has applications in virtual reality and in robotics.

New Insights on Structural Neuroplasticity from MRI

Lecture
Date:
Tuesday, February 15, 2011
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Yaniv Assaf
|
Dept. of Neurobiology Tel Aviv University

Neuro-plasticity is one of the key processes in our brain's physiology. This process allows our brain to change itself, functionally and structurally, following the acquisition of a new skill or experience. While functional aspects of neuro-plasticity can be studied using non-invasive techniques such as fMRI, EEF and MEG, investigation of the structural tissue characteristics of neuro-plasticity requires invasive histological approaches. Long-term experience necessitates structural plasticity which, in the adult brain, is characterized by changes in the shape and number of the synapses (synaptogenesis) as well as other process (neurogenesis, gliogenesis and white matter plasticity). Structural MRI studies of brain plasticity reveal significant volumetric changes via voxel-based morphometry of T1 weighted scans. Yet, the micro-structure correlates of these changes are not well understood. Diffusion tensor imaging (DTI) became one of the most popular imaging techniques in neuroimaging and is regarded as a micro-structural probe. Recently, tract-based spatial statistics (TBSS) analysis of DTI scans before and after long-term motor coordination training (juggling) revealed regional fractional anisotropy (FA) increase in parietal pathways. In that study, FA changes were reported following few weeks of training. An open question is what happens at shorter term learning and memory processes? In a short term spatial navigation study performed both in humans and rodents, we found that diffusion MRI can detect structural changes in cell morphology induced by plasticity within mere hours. Both in humans and rodents, the micro-structural changes, as observed by MRI, were localized to the anticipated brain regions: hippocampus, para-hippocampus, visual cortex, cingulate cortex and insular cortex. Our results indicate that significant structural occur in the tissue within mere hours - an interesting result by itself from the neurophysiological point of view. However, by investigating the induced structural changes both by histology and MRI it is possible to elucidate the relations between tissue micro-structure and the diffusion MRI signal. Preliminary results of such comparison indicate that in gray matter tissue one of cellular correlates of diffusion MRI indices is the density and shape of astrocyte. Indeed more studies should be directed

A new, "sensorimotor", view of seeing

Lecture
Date:
Monday, February 14, 2011
Hour: 14:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. J Kevin O'Regan
|
Laboratoire Psychologie de la Perception CNRS - Université Paris Descartes

There seem to be numerous defects of the eye that would be expected to interfere with vision. Examples are the upside down retinal image, the blind spot in each eye's visual field, non-uniform spatial and chromatic resolution, and blur and image shifts caused by eye saccades. In order to overcome such defects scientists have proposed a variety of compensation mechanisms. I will argue that such compensation mechanism not only face empirical difficulties, but they also suffer from a philosophical objection. They seem to require the existence of a "homunculus" in the brain that contemplates the picture-like output of the compensation mechanism. A new view of what "seeing" consists in is required. The new view of seeing considers seeing as a particular way of actively exploring the environment. This "sensorimotor" approach is subtly different from the idea of "active vision" known today in cognitive or computer science. The sensorimotor approach explains how, despite the eye's imperfections and despite interruptions in the flow of sensory input, we can have the impression of seeing everything in the visual field in detail and continuously. I shall show how the phenomenon of "inattentional blindness" (or "Looked but Failed to See") is expected from the new approach, and I shall examine the phenomenon of "change blindness" which arose as a prediction from the theory. Finally I examine the question of the photographic quality of vision: why we have the impression of seeing things all over the visual field, why everything seems simultaneously and continuously present, and why things seem to visually impose themselves upon us in a way quite different from how memory and imagining do. To explain these facts I shall invoke four objectively measurable aspects of visual interactions: richness, bodiliness, partial insubordinateness and grabbiness.

Reconfiguring Memory

Lecture
Date:
Sunday, February 13, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Shuli Sade
|
Artist, NYC

: Sadé will talk about the relevance in collaboration between artists and scientists, and will introduce her recent art project: “Reconfiguring Memory”. Sadé collaborates with Professor Andre Fenton at NYU Neuroscience labs to develop art for the renovated Neuroscience labs at NYU. Her work with memory, time and light led to this collaboration and will result in art relating to the questions: How does the brain store experience as memories and how the expression of knowledge activates information that is relevant without activating what is irrelevant, and what visual methods can be used for recording the activity of memory, gain or loss.

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Ode To Memory A mini-series devoted to memory in cenema

Lecture
Date:
Tuesday, February 1, 2011
Hour: 14:00
Location:
Dolfi and Lola Ebner Auditorium
Prof. Yadin Dudai
|
Dept of Neurobiology, WIS

Response fluctuations in neurons and networks

Lecture
Date:
Tuesday, February 1, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Prof. Shimon Marom
|
Dept of Physiology Technion Haifa

Experimental analyses of fluctuations in responses to long series of stimuli will be presented. The experiments are performed at the single neuron, population of synapses and network levels. Sources and impacts of these fluctuations will be discussed.

Ode To Memory A mini-series devoted to memory in cinema

Lecture
Date:
Tuesday, January 25, 2011
Hour: 14:00
Location:
Dolfi and Lola Ebner Auditorium
Prof. Yadin Dudai
|
Dept of Neurobiology, WIS

The evolution of behavioral mechanisms: theory and experiments on learning rules and their adaptive (or maladaptive) consequences

Lecture
Date:
Tuesday, January 25, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Prof. Arnon Lotem
|
Dept of Zoology Tel-Aviv University

My talk will be based on our recent attempts to explain apparently maladaptive behaviors in humans and other animals as the consequences of generally adaptive learning mechanisms. I will first describe several cases where seemingly paradoxical behavior can be explained as the result of using relatively simple learning rules. I will then discuss the evolution of such learning rules in the context of individual decision making under variable conditions, as well as in the context of social foraging games of searchers and followers.

Synaptic mechanisms of sensory perception

Lecture
Date:
Wednesday, January 19, 2011
Hour: 10:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Prof. Carl Petersen
|
Brain Mind Institute, EPFL Lausanne, Switzerland

Ode To Memory A mini-series devoted to memory in cinema

Lecture
Date:
Tuesday, January 18, 2011
Hour: 14:00
Location:
Dolfi and Lola Ebner Auditorium
Prof. Yadin Dudai
|
Dept of Neurobiology, WIS

A cellular mechanism for general enhancement of learning capability

Lecture
Date:
Tuesday, January 18, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Dr. Edi Barkai
|
University of Haifa

Learning-related cellular modifications occur not only at synapses but also in the intrinsic properties of the neurons. Learning-induced enhancement in neuronal excitability is evident in hippocampal and piriform cortex pyramidal neurons following a complex olfactory-discrimination operant conditioning task. Such enhanced excitability is manifested in reduced spike frequency adaptation that results from reduction in the slow afterhyperpolarization (AHP), which develops after a burst of action potentials. AHP reduction is apparent throughout the pyramidal cells neuronal population. The AHP amplitude tends to return back to its initial value within days when training is suspended. This recovery is accompanied by reduced learning capability, but not by loss of memories for learned odors. The post-burst AHP reduction is mediated by decreased conductance for a specific calcium-dependent potassium current, the slow IAHP. This long-lasting reduction is dependent on persistent activation of the PKC and ERK second messenger systems. Similar long-lasting AHP reduction can be induced in-vitro by repetitive synaptic stimulation or by kainate application. Such activity-dependent AHP reduction is occluded by prior learning. Olfactory-learning induced enhanced neuronal excitability in CA1 pyramidal neurons is also accompanied by enhanced learning capability in a novel hippocampus-dependent task, the Morris water maze. We suggested that AHP reduction is the cellular mechanism that enables neuronal ensembles to enter into a state which may be best termed "learning mode". This state lasts for up to several days and its behavioral manifestation is enhanced learning capability in tasks that depend on these particular neuronal ensembles. Specifically, enhanced neuronal excitability sets a time window in which most neurons in the relevant neuronal network are more excitable, and thus activity-dependent synaptic modifications are more likely to occur.

What the brain knows about what’s in the nose: Neural processing of pheromone signals

Lecture
Date:
Monday, January 17, 2011
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Dr. Yoram Ben-Shaul
|
Harvard University

Understanding the neuronal events linking sensory inputs with behavioral outputs in complex organisms is a central goal of neuroscience. First steps in this enormous endeavor can be made by focusing on the relatively simple and stereotyped class of chemosensory triggered innately encoded physiological processes. Until recently, analysis of the circuits that underlie these processes was hampered by the lack of a reliable method for stimulus delivery to the vomeronasal system, which in mice, like many other mammals, plays a key role in processing pheromonal information. To address this issue, I developed an experimental preparation that allows in-vivo stimulus delivery to the mouse vomeronasal system and combined it with multisite neuronal recordings to measure stimulus evoked neuronal activity. Recordings from the early processing stage of the accessory olfactory bulb reveal the broad range and high acuity of ethologically relevant sensory representations, and furthermore suggest that these involve integrative processing. Recording from subsequent processing relays in the vomeronasal amygdala reveal several similarities to the olfactory bulb representations but also some intriguing differences raising new hypotheses about the role of the amygdala in these processes. Finally, I will describe how I am extending this approach by employing optogenetic techniques to record neuronal activity from scarce and genetically defined neurons in subsequent processing regions. Taken together, these experiments are beginning to illuminate the function of entire neuronal circuits involved in mediating ethologically and clinically relevant endocrine processes.

Topographic mapping of a hierarchy of temporal receptive windows using natural stimuli

Lecture
Date:
Thursday, January 13, 2011
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Prof. Uri Hasson
|
Dept of Psychology, Princeton University

Space and time are two fundamental properties of our physical and psychological realms. While much is known about the integration of information across space within the visual system, little is known about the integration of information over time. Using two complementary methods of functional magnetic resonance imaging (fMRI) and intracranial electroencephalography (iEEG), I will present evidences that the brain uses similar strategies for integrating information over space and over time. It is well established that neurons along visual cortical pathways have increasingly large spatial receptive fields. This is a basic organizing principle of the visual system: neurons in higher-level visual areas receive input from low level neurons with smaller receptive fields and thereby accumulate information over space. Drawing an analogy with the spatial receptive field (SRF), we defined the temporal receptive window (TRW) of a neuron as the length of time prior to a response during which sensory information may affect that response. As with SRFs, the topographical organization of the TRWs is distributed and hierarchical. The accumulation of information over time is distributed in the sense that each brain area has the capacity to accumulate information over time. The processing is hierarchical because the capacity of each TRW increases from early sensory areas to higher order perceptual and cognitive areas. Early sensory cortices such as the primary auditory or visual cortex have relatively short TRWs (up to hundreds of milliseconds), while the TRWs in higher order areas can accumulate information over many minutes.

Multimodal interactions in primary auditory cortex: Laminar dependence & modulation by general anesthetics

Lecture
Date:
Tuesday, January 11, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Prof. Matthew I. Banks
|
University of Wisconsin, USA

Current theories of the neural basis of sensory awareness suggest that neocortex is constantly comparing expected with observed sensory information. This comparison arises through the integration of ascending inputs from the sensory periphery and descending cortical inputs from the same or other sensory modalities. The importance of this integrative process for awareness is suggested by its selective loss upon anesthetic-induced hypnosis and during slow-wave sleep, but how this integration and its disruption by anesthetics occur within a cortical column is unclear. Using electrophysiological and imaging techniques in rodents in vivo and in brain slices, we show that extrastriate visual cortex provides descending input to primary auditory cortex that modulates responses to auditory stimuli, and that the integration of these information streams is disrupted by general anesthetics.

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