Past events | The department of Brain Sciences

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Distinct layers or a continuum? A morphological and functional analysis of pyramidal cells in the supragranular layers of rat barrel cortex

Lecture

Date:

Thursday, March 10, 2011

Hour: 14:30

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Jochen Staiger

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Dept of Neuroanatomy University of Göttingen

Pyramidal neurons in supragranular layers II and III of rodent sensory cortices are a main target of ascending sensory information conveyed by columnar projections of layer IV as well as contextual information from neighboring columns or higher cortical areas. However, layer II is not separable from layer III on cytoarchitectonic grounds. We therefore investigated to which extent pyramidal neurons in the supragranular layers differ in their input-output connectivity. We obtained detailed spatial maps of layer-specific intracortical functional input connectivity for electrophysiologically and morphologically identified supragranular pyramidal neurons by combining local photolysis of caged glutamate with whole-cell patch-clamp recordings using biocytin-containing pipettes in rat barrel cortex in vitro. The main source of excitatory inputs onto all supragranular pyramidal cells was layer IV of the same column. This translaminar excitatory source was even more prominent than local and transcolumnar excitatory inputs from within the supragranular layers, both in density and strength. Additionally, many pyramidal neurons received a prominent excitatory layer Va input, often originating from beyond the “home” column. Among those pyramidal neurons we detected a significantly higher fraction of cells located in a putative layer II than in TZ or putative layer III. Our results indicate a strong but differential information transmission from layer IV as well as layer Va, both important cortical entry points for parallel streams of sensory information, toward the supragranular layers. Within supragranular layers, information processing in pyramidal neurons can be "fine tuned" through local and transcolumnar excitatory networks. Finally this integrated information is forwarded with a prominent transcolumnar component by putative layer II pyramidal cells but with an intracolumnar preponderance, including significant layer IV-backprojections, by putative layer III pyramidal neurons

Neural correlates of behavior in the rodent striatum

Lecture

Date:

Tuesday, March 8, 2011

Hour: 12:30

Location:

Jacob Ziskind Building

Dr. Dana Cohen

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Gonda Brain Research Center Bar-Ilan University

The striatum consists of GABAergic projection neurons and various types of interneurons. Despite their relative scarcity, these interneurons play a key role in information processing in the striatum. We use multielectrode arrays to record the activity of striatal projection neurons and interneurons in behaving rodents. By comparing their responses we test the ability of the striatum to encode behaviorally relevant information such as movement and context.

The enigma of inflammation in A.L.S: What can be learned from other

Conference

Date:

Sunday, March 6, 2011

Hour:

Location:

Dolfi and Lola Ebner Auditorium

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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

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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

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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

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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

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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

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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

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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.

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All events, All years

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

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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

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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.

Face to Face, Brain to Brain: Exploring the Mechanisms of Dyadic Social Interactions

Lecture

Date:

Thursday, February 3, 2011

Hour: 12:00

Location:

Arthur and Rochelle Belfer Building for Biomedical Research

Prof. Uri Hasson

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Dept of Psychology Princeton University

Cognitive neuroscience experiments typically isolate human or animal subjects from their natural environment by placing them in a sealed quiet room where interactions occur solely with a computer screen. In everyday life, however, we spend most of our time interacting with other individuals. Using fMRI, we recently recorded the brain activity of a speaker telling an unrehearsed real-life story and the brain activity of a listener listening to a recording of the story. To make the study as ecological as possible, we instructed the speaker to speak as if telling the story to a friend. Next, we measured the brain activity of a listener hearing the recorded audio of the spoken story, thereby capturing the time-locked neural dynamics from both sides of the communication. Finally, we asked the listeners to complete a detailed questionnaire that assessed their level of comprehension. Our results indicate that during successful communication the speaker’s and listener’s brains exhibit joint, temporally coupled, response patterns. Such neural coupling substantially diminishes in the absence of communication, for instance, when listening to an unintelligible foreign language. In addition, more extensive speaker–listener neural couplings result in more successful communication. The speaker-listener neural coupling exposes a shared neural substrate that exhibits temporally aligned response patterns across communicators. The recording of the neural responses from both the speaker brain and the listener brain opens a new window into the neural basis of interpersonal communication, and may be used to assess verbal and non-verbal forms of interaction in both human and other model systems.

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

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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

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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

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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

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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

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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

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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

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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.