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On Informational Principles of Embodied Cognition
Lecture
Wednesday, December 29, 2010
Hour: 12:00
Location:
Gerhard M.J. Schmidt Lecture Hall
On Informational Principles of Embodied Cognition
Dr. Daniel Polani
School of Computer Science,
University of Hertfordshire, UK
For many decades, Artificial Intelligence adopted a platonic view that intelligent behaviour is produced in the "brain" only and any body is only an incidental translator between thought and action. In the last two decades, in view of the successes of the subsumption architecture and embodied robotics, this perspective has changed to acknowledge the central importance of the body and the perception-action loop as whole in helping an organisms' brain to carry out useful ("intelligent") behaviours. A central keyword for this phenomenon is, of course, "environmental/morphological computation" (Paul 2006; Pfeifer and Bongard 2007).
The question arises, how/why exactly does this work? What are the principles that make environmental computation work so successfully and how can the contribution that the body provides to cognition be characterized objectively?
In the last years, Information Theory has been identified as providing a natural language to characterize cognitive processing, cognitive invariants as well as the contribution of the embodiment to the cognitive process. The talk will review some highlights of the current state-of-the-art in the field and provide some - sometimes quite surprising - illustrations of the power of the informational view of cognition.
Visual Inference Amid Fixational Eye Movements
Lecture
Tuesday, December 28, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Visual Inference Amid Fixational Eye Movements
Dr. Yoram Burak
Center for Brain Science,
Harvard University
Our visual system is capable of inferring the structure of 2-d images at a resolution comparable (or, in some tasks, greatly exceeding) the receptive field size of individual retinal ganglion cells (RGCs). Our capability to do so becomes all the more surprising once we consider that, while performing such tasks, the image projected on the retina is in constant jitter due to eye and head motion. For example, the motion between two subsequent discharges of a foveal RGC typically exceeds the receptive field size, so the two subsequent spikes report on different regions of the visual scene. This suggests that, to achieve high-acuity perception, the brain must take the image jitter into account. I will discuss two theoretical investigations of this theme.
I will first ask how the visual system might infer the structure of images drawn from a large, relatively unconstrained ensemble. Due to the combinatorially large number of possible images, it is impossible for the brain to act as an ideal observer that performs optimal Bayesian inference based on the retinal spikes. However, I will propose an approximate scheme derived from such an approach, which is based on a factorial representation of the multi-dimensional probability distribution, similar to a mean-field approximation. The decoding scheme that emerges from this approximation suggests a neural implementation that involves two neural populations, one that represents an estimate for the position of the eye, and another that represents an estimate of the stabilized image. I will discuss the performance of this decoding strategy under simplified assumptions on retinal coding. I will also compare it to other schemes, and discuss possible implications for neural visual processing in the foveal region.
In the second part of the talk I will focus on the Vernier task, in which human subjects achieve hyper-acuity, greatly exceeding the receptive field size of a single RGC. The optimal decoder for this task can be formalized and analyzed mathematically in detail. I will show that a linear, perceptron-type decoder cannot achieve hyper-acuity. On the other hand a quadratic decoder, which is sensitive to coincident spiking in pairs of neurons, constitutes an effective and structurally simple solution to the problem. Furthermore, the performance achieved by such a decoder is close to the limit imposed by the ideal Bayesian decoder. Therefore, spike coincidence detectors in the early visual system may facilitate hyper-acuity vision in the presence of fixational eye-motion.
Connectivity and activity of C. elegans locomotion
Lecture
Monday, December 27, 2010
Hour: 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Connectivity and activity of C. elegans locomotion
Dr. Gal Haspel
National Institute of Neurological Disorders and Stroke, NIH
I study the neuronal basis of locomotion in the nematode C elegans. With only 302 neurons in its nervous system, 75 of which are locomotion motorneurons, C. elegans offers a tractable network to study locomotion. In this talk I will describe my research, which uses a neuroethological approach to study both the behavior and the underlying connectivity and activity of neurons and muscle cells.
Genetic dissection of rheumatoid arthritis – the end of the beginning
Lecture
Monday, December 27, 2010
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Genetic dissection of rheumatoid arthritis – the end of the beginning
Dr. Katherine Siminovitch
Mount Sinai Hospital
Toronto, Ontario
In this talk I will review the rationale for searching for autoimmune disease susceptibility genes and in particular for genes conferring risk for rheumatoid arthritis(RA). I will then review the current state of knowledge on RA genes and will then focus on one of the few newly-discovered genes (PTPN22) for which we know the disease causal gene variant. This gene encodes a tyrosine phosphatase ,LYP, and I will present recent data from my lab in which we use an animal model to show how the RA-associated PTPN22/LYP variant causes T cell dysfunction that could predispose to autoimmunity.
Optogenetic deconstruction of the neuronal circuits underlying dynamic retrieval strategies for long-term memories
Lecture
Tuesday, December 21, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Optogenetic deconstruction of the neuronal circuits underlying dynamic retrieval strategies for long-term memories
Dr. Inbal Goshen
Dept of Bioengineering,
Stanford University, Stanford CA
Cognitive function and emotional homeostasis, and the aspiration to decipher their neuronal basis have stood at the heart of neuroscience since its inception. The complexity of the circuits underlying these processes is immense, and new techniques are necessary to provide novel efficient ways to make a significant progress in brain research. Optogenetic tools enable temporally and spatially precise in-vivo activation or inactivation of genetically defined cell populations, thus enabling deconstruction of systems that were not available for research. An example for that is my work re-examining the role of the hippocampus in remote memory. The prevailing theory suggests that the process of remote memory consolidation requires early involvement of the hippocampus, followed by the neocortex. In the course of this process, an influence of hippocampus on neocortex may enable the hippocampus to facilitate the remote cortical storage of memory, rather than stably store the memory itself. Indeed, contextual fear memories in rodents are completely unaffected by hippocampal lesions or pharmacological inhibition on the remote timescale of weeks after training, but do depend on the hippocampus over the recent timescale of days after training. However, in exploring the contribution of defined cell types to remote memory using optogenetic methods (which are orders of magnitude faster in onset and offset than earlier methods), we found that even weeks after contextual conditioning, the contextual fear memory recall could be abolished by optogenetic inhibition of excitatory neurons in the CA1 region of the hippocampus- at times when all earlier studies had found no detectable influence of hippocampus. We also optogenetically confirmed the remote-timescale importance of anterior cingulate cortex. In exploring mechanisms, we found that loss of hippocampal involvement at remote timepoints depended on the timescale of hippocampal inhibition, since 1) we replicated earlier pharmacological work using longer-lasting drug-mediated inhibition of hippocampus (revealing the recent, but not remote, effects on memory); and 2) extending optogenetic inhibition of hippocampus to match typical pharmacological timescales converted the remote hippocampus-dependence to remote hippocampus-independence. These findings uncover a remarkable dynamism in the mammalian memory retrieval process, in which underlying neural circuitry adaptively shifts the default structures involved in memory—normally depending upon the hippocampus even at remote timepoints, but flexibly moving to alternate mechanisms when the hippocampus is offline on the timescale of minutes. This new model is further supported by the finding that contextual memory was instantaneously suppressed by CA1 inhibition even in the midst of a single freely-moving behavioral session, after the memory was already retrieved. Our findings have broad implications for the interpretation of drug or lesion data in other systems, and may open an exciting therapeutic avenue for PTSD patients, in which a pathology-inducing contextual memory could be stopped as it appears without permanently affecting other memories.
Anesthesia: a window to the neuronal activity underlying consciousness
Lecture
Tuesday, December 7, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Anesthesia: a window to the neuronal activity underlying consciousness
Dr. Aeyal Raz
Dept of Anesthesia
Rabin Medical Center
The neural mechanisms underlying consciousness have been one of the most intriguing yet elusive questions facing science. We will discuss how the activity of the neuronal population changes during loss of consciousness following administration of general anesthesia drugs.
We measured the changes of Sub-thalamic nucleus neurons activity during administration of propofol (GABAA agonists) and Remifentanil (opiate agonist). This was done during implantation of deep brain stimulation electrodes for the treatment of Parkinson’s disease in humans. Administration of both Propofol and remifentanil leads to a similar reduction of STN multi-unit neuronal spiking activity. Remifentanil seems to interfere with the oscillatory pattern of STN activity whereas propofol does not.
In order to broaden our understanding of the effect of anesthetic drugs, we performed extra-cellular recordings of neuronal activity from the cortex and globus pallidus of vervet monkeys using multiple electrodes. The recordings were performed during sedation with Ketamine (NMDA antagonist). Our results demonstrate the appearance of synchronous oscillatory activity of the LFP at slow (<1 Hz) delta (3-4Hz) and gamma (35-50Hz) in the motor cortex and globus pallidus following ketamine injection and loss of consciousness. These oscillations are synchronized between regions as well, and are correlated to the spiking activity of neurons in these regions.
We propose that loss of consciousness following anesthesia is due to the appearance of synchronized oscillatory activity in different regions of the brain, preventing the normal processing and passage of information.
Acquired alternative splicing changes in Alzheimer's and Parkinson's diseases
Lecture
Tuesday, November 30, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Acquired alternative splicing changes in Alzheimer's and Parkinson's diseases
Prof. Hermona Soreq
Safra Center of Neuroscience
The Hebrew University of Jerusalem
Multiple lines of evidence link numerous diseases to inherited errors in alternative splicing, the process connecting different exon and intron sequences to diversify gene expression. We explore potential involvement of acquired alternative splicing changes in non-familial Alzheimer's and Parkinson's diseases (AD, PD), where synaptic functioning fails and cholinergic or dopaminergic neurons die prematurely. Using whole genome microarrays, we found massive decline in exon exclusion events in the AD entorhinal cortex. In brain-injected mice, blocking exon exclusion caused learning and memory impairments and destruction of cholinergic neurons caused AD-like changes in exon exclusion. Suggesting physiological relevance, blocking exon exclusion in primary neuronal cells was preventable by cholinergic stimulation and caused dendritic and synapse loss. In comparison, blood leukocytes from advanced PD patients showed different alternative splicing changes. These were largely reversed by deep brain stimulation (DBS), which reduces motor symptoms, and were reversed again after disconnecting the stimulus. Measured modifications correlated with neurological treatment efficacy and classified controls from advanced PD patients and pre- from post-surgery patients. In an independent patient cohort, a "molecular signature" (6 out of the modified transcripts) further classified controls from patients with early PD or other neurological diseases. Our findings demonstrate functionally relevant disease-specific alternative splicing changes in the AD brain and PD leukocytes; highlight acquired alternative splicing changes as causally involved in different neurodegenerative diseases and identify new targets for intervention in DBS-treatable neurological diseases.
Visualizing Circuits in the Visual System
Lecture
Thursday, November 25, 2010
Hour: 12:00
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Visualizing Circuits in the Visual System
Prof. Josh Sanes
Center for Brain Science
Harvard University
Formation of neural circuits requires that axons recognize appropriate cells, and even appropriate parts of cells, upon which to synapse. In the retina, amacrine and bipolar cells form synapses on retinal ganglion cells (RGCs) in the inner plexiform layer (IPL). The visual features to which different RGC subtypes respond depend on what input they receive, prime determinants of which are the IPL sublaminae in which their dendrites make synapses. We have therefore sought molecules that mark RGC subtyoes and mediate lamina-specific connectivity. Candidates include members of the immunoglobulin superfamily, such as Sidekicks, Dscams and JAMs, and members of the cadherin superfamily, such as Class II and protocadherins. I will discuss our progress toward identifying and testing such candidates. I will also discuss methods for tracing connections of retinal neurons in wild-type and mutant mice, so that we can assess the consequences of perturbing target recognition systems.
Cortical blood flow: Every (subsurface) vessel counts
Lecture
Wednesday, November 24, 2010
Hour: 11:00
Location:
Gerhard M.J. Schmidt Lecture Hall
Cortical blood flow: Every (subsurface) vessel counts
Prof. David Kleinfeld
Dept of Physics
University of California at San Diego La Jolla, CA
Neuronal processing has a high energetic cost, all of which is supplied through brain vasculature. What are the design rules for this system? How is flow controlled by neuronal activity? How do neurons respond to failures in the vasculature? Theses questions will be addressed at the level of necortex in rat and mouse. An essential aspect of this work is the use of nonlinear optical tools to measure and perturb vasodynamics and automate the large-scale mapping of brain angioarchitecture.
The neurobiology of seizures and depression
Lecture
Tuesday, November 23, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
The neurobiology of seizures and depression
Dr. Oscar G. Morales
Associate Director, Psychiatric Neurotherapeutics Program (PNP)
Harvard Medical School
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Individual differences in the expression and control of conditioned fear
Lecture
Sunday, August 15, 2010
Hour: 12:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Individual differences in the expression and control of conditioned fear
Catherine Hartley
Doctoral Student, New York University
In order to function adaptively in a complex environment, individuals must both react to environmental threats and modify their reactions as circumstances change. A large body of work employing Pavlovian conditioning paradigms has generated a detailed neuroscientific understanding of how fear responses are acquired. More recent research has begun to probe the various means by which learned fear can be diminished. The vast majority of this research focuses on the mechanisms that underlie typical responding in an idealized “average” individual. A robust model of fear learning must also account for the substantial variability in fear reactivity and regulation that exists between individuals. The experiments presented here explore neurobiological and experiential factors that are associated with individual variation in the expression and regulation of conditioned fear using psychophysiology, neuroimaging, and behavioral genetics.
Faces, Attention, and the Temporal Lobe
Lecture
Thursday, August 12, 2010
Hour: 11:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Faces, Attention, and the Temporal Lobe
Prof. Winrich Freiwald
The Rockefeller University, New York
Understanding the neural mechanisms of visual object recognition is a difficult task in part, because for any given object it is not clear, which exact part of the brain to study. Yet evolution has presented us with a unique model system to decipher these mechanisms. The temporal lobes of macaque monkeys contain neural machinery to support face recognition consisting of six discrete patches of face-selective cortex. The two main organizing features of this system – concentration of cells encoding the same complex object category into modules and spatial separation of modules – make it possible to break down the process of face recognition into its components. In my talk I will present anatomical results supporting the notion that the distributed face patches really are part of an integrated face-processing machine, and electrophysiological results showing that each patch subserves a distinct computational function. In the second part of my talk I will turn to something completely different, attention. Using fMRI in macaque monkeys, we found a network of areas to be modulated by attention in motion-discrimination task, included a hitherto unsuspected region within inferotemporal cortex, PITd. We then targeted PITd for electrophysiological recordings and electrical microstimulation in different tasks to learn about its role in sensory information processing and spatial attention. I will discuss the somewhat radical conclusion we arrived at, namely that PITd may constitute a region for attentional control.
Embraining the mind: On cerebral localization and the nature of culture
Lecture
Monday, August 9, 2010
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Embraining the mind: On cerebral localization and the nature of culture
Dr. Sky Gross
Dept of Sociology and Anthropology
Tel Aviv University
Are we our brains?
This question has troubled Western society for centuries, and still does today. Philosophers, psychologists, psychiatrists and neuroscientists - as much as the lay public - battle with the question of whether our personality, sense of self and states of mind can truly be explained through a scientific study of the brain, and whether one can at least correlate these with brain activity and structure. With the recent hyperbolic advances made in neuroscience, these questions arise in the form of intensive and broad debates on whether one may be able, at some point in the future, to fully account for what we cherish more than all, our sense that we are more than a lump of flesh.
This "more" however, does not belong to the realm of science: in the laboratory, one must deal with observable and operalizationable phenomena – everything core subjectivity ('qualia'- e.g. the experience of pain, of seeing the color red) is not. How can neuroscience approach the mind without losing its brain? How well has it done thus far, and what may we expect in the future?
This talk will suggest one – among many – approaches to this quandary, by looking at the history and current practices of brain localization. By introducing the mind-body conundrum into the study of this enterprise, we will consider the extent to which localization and classification of brain/mind functions serve as a way to materialize what is/was believed to be beyond 'matter'. The following debate will allow a discussion of an issue that concerns us all.
Translational Research in the Neuroscience of Fear Extinction: Implications to PTSD and Other Anxiety Disorders
Lecture
Wednesday, July 14, 2010
Hour: 15:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Translational Research in the Neuroscience of Fear Extinction: Implications to PTSD and Other Anxiety Disorders
Prof. Mohammed Milad
Psychiatry Dept, Harvard Medical School and Massachusetts General Hospital, Charlestown, MA
Some people adapt well in the aftermath of traumatic events and are quickly able to inhibit their fear responses to trauma-associated stimuli. Fear responses, however, persist for longer periods of time for others to the point where they reach a pathological state. Why are some people more resilient to trauma while others are not? What are the neural substrates that underlie fear inhibition and extinction? Are these circuits deficient in patients with anxiety disorders? In my talk, I will focus on presenting translational data from the rat and human brains with the objective of trying to provide some preliminary answers to the above stated questions. Specifically, I will review human studies indicating that prefrontal areas homologous to those critical for extinction in rats. Furthermore, I will present some data to show that those brain regions in the rat brain appear to be structurally and functionally homologous to specific brain regions in the human brain. I will also show some data suggesting that these brain regions, the ventromedial prefrontal cortex (vmPFC) and the dorsal anterior cingulate cortex (dACC), appear to be deficient in patients with posttraumatic stress disorder (PTSD). I will present some structural and functional neuroimaging and psychophysiological studies done in our lab that focused on the neural mechanisms of fear extinction, particularly extinction recall and the contextual modulation of extinction recall. These recent studies suggest that: 1) human vmPFC is involved in the recall of extinction memory; 2) the size of the vmPFC might explain individual differences in the ability to modulate fear among humans; 3) hippocampal activation is observed during the recall of extinction memory in a context where extinction training took place but not in the initial conditioning context; 4) and the dACC may be involved in the expression of fear responses. I will also present recent neuroimaging and psychophysiological data from PTSD patients suggesting that 1) the retention of extinction memory is impaired in PTSD, and 2) the function of the vmPFC and dACC (measured by fMRI) appears to be impaired in PTSD in the context of fear extinction. Implications of these findings to the pathophysiology of anxiety disorders such as PTSD and current extinction-based behavioral therapies for anxiety disorders will be discussed.
Active sensing in echolocating bats: What we know and what we would like to know
Lecture
Tuesday, June 29, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Active sensing in echolocating bats: What we know and what we would like to know
Yossi Yovel
Postdoc, Ulanovsky Group, Dept of Neurobiology, WIS
All sensory systems are active to some extent. Echolocating bats, which rely on their own emitted energy to perceive the surroundings, probably employ the most tightly-controlled active sensing system. The sensory degrees of freedom that bats can control are commonly divided into three categories: Timing, Signal design, and Directionality. In this talk, I will address all three categories and will summarize what we already understand and what we would love to understand.
Estrogen Attenuates Ischemic Oxidative Damage via Inhibition of NADPH Oxidase Activation Role of Estrogen-Induced Neuroprotection:
Lecture
Thursday, June 24, 2010
Hour: 10:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Estrogen Attenuates Ischemic Oxidative Damage via Inhibition of NADPH Oxidase Activation Role of Estrogen-Induced Neuroprotection:
Limor Raz
Institute of Molecular Medicine & Genetics,
Developmental Neurobiology Program,
Dept of Neurology, Medical College of Georgia, Augusta, GA, USA
17-β estradiol (E2) has been implicated to be neuroprotective, yet the mechanisms underlying E2-mediated protection against stroke remains unclear. The purpose of the current study was to elucidate the role of E2 in NADPH oxidase (NOX2) activation during ischemia/reperfusion induction of superoxide in the hippocampus CA1 region following global cerebral ischemia (GCI) and to explore the regulation of downstream proapoptotic factors by E2. Using a 4-vessel occlusion model to induce GCI, we showed that neuronal NOX2 localizes to the membrane and that NADPH oxidase activity and superoxide production were rapidly and markedly attenuated by E2 following reperfusion. Inhibition of NADPH oxidase activation via icv administration of a NOX2 competitive inhibitor, gp91ds-tat, strongly attenuated superoxide production and was neuroprotective. The increase of neuronal NADPH oxidase and superoxide following cerebral ischemia was shown to require Rac1 activation, as administration of a Rac1 inhibitor (NSC23766) significantly attenuated NADPH oxidase activation and superoxide production following stroke. NSC23766 treatment was also neuroprotective and improved spatial learning and memory. Interestingly, treatment with the competitive NOX2 inhibitor (Gp91ds-tat), but not the scrambled tat peptide control, attenuated acetylation of downstream p53 and reduced levels of the P53 transcriptional target and apoptotic factor, PUMA. Taken as a whole, our studies reveal a novel, membrane-mediated antioxidant mechanism of E2-induced neuroprotection via reduction of neuronal NOX2 activation, superoxide production and neuronal cell death in the hippocampus CA1 following cerebral ischemia.
Chemosensory dysfunction in humans
Lecture
Sunday, June 20, 2010
Hour: 10:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Chemosensory dysfunction in humans
Prof. Thomas Hummel
Smell and Taste Clinic, Dept of Otorhinolaryngology
University of Dresden Medical School, Dresden
Abstract: The intent of this presentation is to help bridge the gap between the clinical realm and the research laboratory. The clinical literature has a growing mass of evidence showing how disorders such as epilepsy, Alzheimer’s disease, stroke, or surgically-induced injury to peripheral nerve, can have devastating effects on olfactory and gustatory functions. A loss of function might be an early symptom with diagnostic value that helps the clinician identify the disease state. The presentation will introduce the non-clinician to common diagnostic and experimental tests of olfactory and taste functions. Various causes of olfactory loss will be discussed, plus their therapy
Optimal adaptation of retinal processing to color contrasts
Lecture
Tuesday, June 15, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Optimal adaptation of retinal processing to color contrasts
Dr. Ronen Segev
Life Sciences Dept
Ben Gurion University of the Negev
The visual system continually adjusts its sensitivity to properties of the environment. This adaptation process starts in the retina, which encodes over 8 orders of magnitude of light intensity using a limited range of spiking outputs of the ganglion cell, the only cells to project axons to the brain, extending between zero to several hundreds spikes per second. While the different spectral sensitivities of photoreceptors give the first separation of color channels in the visual system, chromatic adaptation observed in psychophysical experiments is commonly thought to originate from high visual areas. We show that color contrast adaptation actually starts in the retina by ganglion cells adjusting their responses to spectral properties of the environment. Specifically, we demonstrate that the ganglion cells match their response to red-blue stimulus combinations according to the relative contrast of each of the input channels. Using natural scene statistics analysis and theoretical consideration, we show that the retina balances inputs from the two color channels optimally given the strong correlation between the long and short wavelengths in the natural environment. These results indicate that some of the sophisticated processing of spectral visual information attributed to higher visual processing areas can be actually performed by the retina.
Contrast Tuning in Face Cells
Lecture
Sunday, June 13, 2010
Hour: 12:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Contrast Tuning in Face Cells
Shay Ohayon
Graduate Student, Computation and Neural Systems, CALTECH
Several state-of-the-art computer vision systems for face detection, e.g., Viola-Jones [1], rely on region-based features that compute contrast by adding and subtracting average image intensity within different regions of the face. This is a powerful strategy due to the invariance of these features across changes in illumination (as proposed by Sinha [2]). The computational mechanisms underlying face detection in biological systems, however, remain unclear. We set to investigate the role of region-based features in the macaque middle face patch, an area that consists of face-selective neurons. We found that individual neurons were tuned to subsets of contrast relationships between pairs of face regions. The sign of tuning for these relationships was strikingly consistent across the population (for example, almost all neurons preferred a lower average intensity in the eye region relative to the nose region). Furthermore, the pairs and polarity of tuning were fully consistent with Sinha’s proposed ratio-template model of face detection [2]. Non-face images from the CBCL dataset that contained correct contrast polarities in pre-defined regions (facial parts) did not elicit increased firing in face-selective neurons, suggesting that the neurons are not only computing averaged intensity according to a fixed template, but are also sensitive to the specific shape of features within a region.
[1] Robust Real-time Object Detection, Paul Viola and Michael Jones.
Second International Workshop on Statistical and Computational Theories of Vision – Modeling, Learning, Computing, and Sampling.
Vancouver, Canada, July, 2001.
[2] Qualitative Representations for Recognition, Pawan Sinha. Proceedings of the Second International Workshop on Biologically
Motivated Computer Vision, Tubingen, November, 2002.
Sensory Coding and Decoding for Smooth Pursuit Eye Movements
Lecture
Thursday, June 10, 2010
Hour: 18:00
Location:
Nella and Leon Benoziyo Building for Brain Research
Sensory Coding and Decoding for Smooth Pursuit Eye Movements
Prof. Stephen Lisberger
Dept of Physiology
University of California San Francisco
Featured Review:
Visual Guidance of Smooth-Pursuit Eye Movements: Sensation, Action, and What Happens in Between
S.G. Lisberger
Smooth pursuit eye movements transform visual motion into a rapid initiation of eye movement and sustained accurate tracking. The pursuit response is encoded in distinct responses of neural circuits for visual motion in area MT, implemented in the cerebellum and the smooth eye movement region of the frontal eye fields and controlled by volition on a rapid time scale. Lisberger reviews the features that make pursuit a model system for studying the general principles of sensory-motor processing in brain.
http://www.cell.com/neuron/abstract/S0896-6273%2810%2900198-4
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