2011
, 2011
Lazy Neurons for Good Shape or Filling in the Gaps...The Mind's Way
Lecture
Tuesday, March 15, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Lazy Neurons for Good Shape or Filling in the Gaps...The Mind's Way
Dr. Ohad Ben-Shahar
Dept of Computer Science
Ben Gurion University
The phenomenon of visual curve completion, where the visual system completes the missing part (e.g., due to occlusion) between two contour fragments, is a major problem in perceptual organization research, both behaviorally and computationally. Previous computational approaches for the shape of percetually completed curves typically follow an axiomatic approach via formal descriptions of desired, image-based perceptual properties (e.g, minimum total curvature, roundedness, etc...). Unfortunately, however, it is difficult to determine such desired properties psychophysically and indeed there is no consensus in the literature for what they should be. Instead, in this paper we suggest to exploit the fact that curve completion occurs in early vision in order to formalize the problem in a space that abstracts the primary visual cortex (For the technically inclined, this space is called the unit tangent bundle associated with R2). We show that a single basic principle of “minimum energy consumption” in this space not only results in a rigorous, non axiomatic, computational theory, but also makes excellent predictions and explanations for recent perceptual findings in the literature
Distinct layers or a continuum? A morphological and functional analysis of pyramidal cells in the supragranular layers of rat barrel cortex
Lecture
Thursday, March 10, 2011
Hour: 14:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Distinct layers or a continuum? A morphological and functional analysis of pyramidal cells in the supragranular layers of rat barrel cortex
Prof. Jochen Staiger
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
Tuesday, March 8, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Neural correlates of behavior in the rodent striatum
Dr. Dana Cohen
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
Sunday, March 6, 2011
Hour:
Location:
Dolfi and Lola Ebner Auditorium
Measuring Behavior and Physiology: Bridging the Genotype Phenotype Gap
Conference
Thursday, March 3, 2011
Hour: 08:00 - 16:30
Location:
Dolfi and Lola Ebner Auditorium
Stimulus-specific adaptation – beyond the oddball paradigm
Lecture
Tuesday, March 1, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Stimulus-specific adaptation – beyond the oddball paradigm
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
Wednesday, February 23, 2011
Hour: 15:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Deletion of the mouse genomic interval corresponding to human 16p11.2 causes autism-like phenotypes
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
Tuesday, February 22, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Pavlovian-like behavior in microbes
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
Monday, February 21, 2011
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Mechanisms of vocal learning in the songbird: A hypothesis for the role of cortical-basal ganglia circuits
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
Sunday, February 20, 2011
Hour: 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Unraveling the structure of time in the brain
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.
Pages
2011
, 2011
Neural correlates of behavior in the rodent striatum
Lecture
Tuesday, March 8, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Neural correlates of behavior in the rodent striatum
Dr. Dana Cohen
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.
Stimulus-specific adaptation – beyond the oddball paradigm
Lecture
Tuesday, March 1, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Stimulus-specific adaptation – beyond the oddball paradigm
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
Wednesday, February 23, 2011
Hour: 15:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Deletion of the mouse genomic interval corresponding to human 16p11.2 causes autism-like phenotypes
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
Tuesday, February 22, 2011
Hour: 12:30
Location:
Jacob Ziskind Building
Pavlovian-like behavior in microbes
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
Monday, February 21, 2011
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Mechanisms of vocal learning in the songbird: A hypothesis for the role of cortical-basal ganglia circuits
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
Sunday, February 20, 2011
Hour: 11:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Unraveling the structure of time in the brain
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
Wednesday, February 16, 2011
Hour: 11:00
Location:
Gerhard M.J. Schmidt Lecture Hall
A sensorimotor account of phenomenal consciousness
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
Tuesday, February 15, 2011
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
New Insights on Structural Neuroplasticity from MRI
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
Monday, February 14, 2011
Hour: 14:00
Location:
Gerhard M.J. Schmidt Lecture Hall
A new, "sensorimotor", view of seeing
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
Sunday, February 13, 2011
Hour: 12:30
Location:
Gerhard M.J. Schmidt Lecture Hall
Reconfiguring Memory
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.
Pages
2011
, 2011
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