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Altered Function of the Prefrontal Cortex Following Extended Access to Self-Administered Cocaine
Lecture
Monday, November 8, 2010
Hour: 13:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Altered Function of the Prefrontal Cortex Following Extended Access to Self-Administered Cocaine
Dr. Osnat Ben-Shahar
Dept of Psychology
University of California Santa Barbara
One main alteration in neural function observed in human cocaine addicts is reduced function in the medial prefrontal cortex (mPFC). However, whether altered function of the mPFC precede, or result from, excessive self-administration of cocaine, and the exact neurochemical changes it consists of, is still unknown. To answer these questions, one needs an appropriate animal model of addiction. As, it is well established that differences in the route of, and control over, cocaine-administration, or in the frequency and size of the daily-dose of cocaine, result in significant differences in cocaine-induced neurochemical effects; then if we are to better understand the neuroadaptations that underlie the development of addiction in humans, we should employ animal models that mimic as closely as possible the human situation. Hence, my lab utilize an animal model that employs intravenous self-administration of cocaine, under conditions (based on Ahmed & Koob, 1998) that distinguish the effects of brief versus extended daily access to cocaine upon both behavior and neural substrates. This permits the investigation of neuroadaptations associated with the transition from the drug-naïve state to controlled drug-use, versus the further adaptations associated with the transition from controlled to compulsive drug-use. Using this model, we measured basal, as well as cocaine-induced, release of glutamate and dopamine within the mPFC during and after various levels of exposure to cocaine. The differences we found between controlled and compulsive drug-states, will be discussed in this talk.
HOW RHYTHMIC ACTIVITIES IN THE BRAIN MAKE YOU FEAR AND FORGET
Lecture
Tuesday, October 12, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
HOW RHYTHMIC ACTIVITIES IN THE BRAIN MAKE YOU FEAR AND FORGET
Prof. Hans-Christian Pape
Institute for Physiology I
Westfälische Wilhelms University Münster, Germany
Fear is a crucial adaptive component of the behavioral repertoire that is generated in relation to stimuli which threaten to perturb homeostasis. Fear-relevant associations are learned and consolidated as part of long term memory. After learning, fear responses are modulated through processes termed safety learning and extinction. Perturbation of these mechanisms can lead to disproportional anxiety states and anxiety disorders. Recent years have seen considerable progress in identifying relevant brain areas – such as the amygdala, the hippocampus and the prefrontal cortex - and neurophysiological principles. Key mechanisms, involving rhythmic oscillations of neuronal subpopulations and neuromodulatory influences, will be discussed
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.
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Generalizing Learned Movement Skills from Infancy to Maturity
Lecture
Tuesday, June 8, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Generalizing Learned Movement Skills from Infancy to Maturity
Dr. Eilat Almagor
A Feldenkrais Trainer
The Rubin Academy of Music and Dance, Jerusalem
During the first year of life, babies learn skills of movement which serve them not only for their present stage, but are building blocks for future stages. There are special qualities of the learning process in early development stages, which allow the learned experiences to be generalized in later stages.
For example the skills that are learned in horizontal locomotion (crawling) are also applied in walking. This learning process is playful and rich with mistakes It is complex in the sense that at each moment there is an overlap of a few functions. For example, keeping the balance while lifting a toy.By observing video clips of a few babies playing, we will see some of the necessary qualities of the learning process.
We will also see movement lessons given to disabled children, providing them with the normal ingredients of the learning process, in spite of their disabilities.
Neuronal deficits in mouse models of Alzheimer's disease: structure, function, and plasticity
Lecture
Tuesday, June 1, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Neuronal deficits in mouse models of Alzheimer's disease: structure, function, and plasticity
Dr. Edward Stern
Brain Research Center,
Bar-Ilan University,
Associate in Neurobiology, Massachusetts General Hospital,
Assistant Professor of Neurology, Harvard Medical School
In the 104 years since Alois Alzheimer first described the neuropathological features underlying dementia in the disease that now bears his name, the changes in neuronal activity underlying the symptoms of the disease are still not understood. Using transgenic mouse models, it is now possible to directly measure changes in neuronal structure and function resulting from the accumulation of AD neuropathology.
We measured the changes in evoked responses to electrical and sensory stimulation of neocortical neurons in mice transgenic for human APP, in which soluble amyloid-β accumulates and insoluble plaques aggregate in an age-dependent manner. Our results reveal a specific synaptic deficit present in neocortical neurons in brains with a significant amount of plaque aggregation. We show that this deficit is related to the distortion of neuronal process geometry by plaques, and the degree of response distortion is directly related to the amount of plaque-burdened tissue traversed by the afferent neuronal processes, indicating that the precise connectivity of the neocortex is essential for normal information processing. Furthermore, we show that the physical distortion of neuronal processes by plaques is reversible by immunotherapy, revealing a larger degree of structural plasticity in neocortical neurons of aged animals. Taken together, these results indicate that it may be possible to slow or reverse the symptoms of AD.
Neuronal Response Clamp
Lecture
Sunday, May 30, 2010
Hour: 14:30
Location:
Nella and Leon Benoziyo Building for Brain Research
Neuronal Response Clamp
Avner Wallach
Network Biology Research Laboratories, Technion
Guest Student, Ahissar Group, Dept of Neurobiology, WIS
Since the first recordings made of evoked action potentials it has become apparent that the responses of individual neurons to ongoing physiologically relevant input, are highly variable. This variability is manifested in non-stationary behavior of practically every observable neuronal response feature. We introduce the Neuronal Response Clamp, a closed-loop technique enabling full control over two important single neuron activity variables: response probability and stimulus-spike latency. The technique is applicable over extended durations (up to several hours), and is effective even on the background of ongoing neuronal network activity. The Response Clamp technique is a powerful tool, extending the voltage-clamp and dynamic-clamp approaches to the neuron's functional level, namely-its spiking behavior.
The Hippocampus in Space and Time
Lecture
Thursday, May 27, 2010
Hour: 14:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
The Hippocampus in Space and Time
Prof. Howard Eichenbaum
Center for Memory and Brain
Boston University
In humans, hippocampal function is generally recognized as supporting episodic memory, whereas in rats, many believe that the hippocampus creates maps of the environment and supports spatial navigation. Is this a species difference, or is there a fundamental function of the hippocampus that supports cognition across species? Here I will discuss evidence that hippocampal neuronal activity in spatial memory is more related to the representation of routes than the maps, suggesting a potential function of the hippocampus in memory for unique sequences of events. Further studies support this view by showing that the hippocampus is critical to memory for sequential events in non-spatial episodic memories. Correspondingly, neural ensemble activity in the hippocampus involves a gradually changing temporal context representation onto which specific events might be coded. Finally, at the level of single-neuron spiking patterns, hippocampal principal cells encode specific times within spatial and non-spatial sequences (“time cells”, as contrasted with “place cells”), and encode specific events within sequence memories onto the representation of time. These findings support an emerging view that the hippocampus creates “scaffolding” for memories, representing events in their spatial and temporal context.
Associative Cortex in the First Olfactory Brain Relay Station?
Lecture
Thursday, May 13, 2010
Hour: 13:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Associative Cortex in the First Olfactory Brain Relay Station?
Prof. Diego Restrepo
Director, Neuroscience Program
Department of Cell and Developmental Biology
University of Colorado, Denver, CO
Synchronized firing of mitral cells in the olfactory bulb, the first relay station of the olfactory system, has been hypothesized to convey information to olfactory cortex. In this first survey of synchronized firing by mitral cells in awake behaving vertebrates, we find sparse divergent odor responses. Surprisingly, synchronized firing conveys information on odor value (is it rewarded?) rather than odor quality. Further, adrenergic block decreases the magnitude of odor divergence of synchronous firing. These data raise questions whether mitral cells contribute to decision-making, or convey expected outcomes used in prediction error calculation.
Sculpting the hippocampal cognitive map: experimental control over the coded parameter space
Lecture
Tuesday, May 11, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Sculpting the hippocampal cognitive map: experimental control over the coded parameter space
Dr. Genela Morris
Dept of Neurobiology and Ethology
University of Haifa
Although much work in the field of reinforcement learning has been devoted to understanding how animals and humans learn to perform the best action in each state of affairs, strikingly scant work targets the question of what constitutes such a state. In initial phases of learning, an animal or a person cannot know which facets of its rich experience should be attended to in order to identify their ‘state’. In a number of projects, we use tasks in which several different attributes can potentially be important for procuring rewards (odors, spatial location, previous actions), and specifically investigate the behavioral and neural processes underlying learning of which is the relevant state. This talk will focus on parameter coding by hippocampal primary neurons.
The hippocampus serves an important role in learning and memory. In humans, it is associated with declarative episodic memory. Single unit recordings of hippocampal neurons in freely behaving rats have shown that many of them act as place-cells, confining their firing to well-defined locations in space. We recorded the activity of hippocampal primary neurons in a specially devised olfactory space, in which rats foraged for reward based solely on olfactory cues and studied the dependence of the activity of these neurons on their availability. We show that place cells shifted their firing fields from room coordinates to olfactory coordinates as animals learned to rely on them in order to obtain reward.
The use of olfactory cues provides the additional benefit of careful control over the sensory inputs provided to the animals. Classical studies on hippocampal place-cells show that when the environment is visually altered, these hippocampal neurons 'remap', in a seemingly random manner. Although studies have been conducted to investigate the contribution of various visual aspects to the activity of place cells, the exact correlation of hippocampal cell firing to the visual input to the rats cannot be studied in freely behaving rats, because their field of view is unknown. By repeating the sequence of olfactory stimuli provided in the maze in a new environment, we study the relation between the neuronal responses of single neurons to given sensory stimuli in distinct spatial contexts. Preliminary results suggesting that the mapping of hippocampal neurons is not random, but critically depends on the sequence in which the different items are encountered, in support of the relational representation theory of hippocampal function.
Memory encoding and retrieval:A hippocampal “place-field centric” perspective
Lecture
Monday, May 10, 2010
Hour: 12:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Memory encoding and retrieval:A hippocampal “place-field centric” perspective
Prof. Etan Markus
Dept of Psychology
University of Connecticut
As a rat runs through a familiar environment, the hippocampus retrieves a previously stored spatial representation of the environment. When the environment is modified a new representation is seen, presumably corresponding to the hippocampus encoding the new information. I will present single unit data and discuss how the “hippocampus decides” whether to retrieve an old representation or form a new representation.
Synaptic and local circuit plasticity in the dentate gyrus – potential relevance to traumatic memories
Lecture
Tuesday, May 4, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Synaptic and local circuit plasticity in the dentate gyrus – potential relevance to traumatic memories
Prof. Gal Richter-Levin
The Brain and Behavior Research Center
University of Haifa
Synopsis: Depending on its severity and context, stress can affect neural plasticity. Most related studies focused on synaptic plasticity and long-term potentiation (LTP) of principle cells. However, evidence suggests that following stress, modifications can also take place at the level of complex interactions with interneurons, i.e. at the local circuit level. We set out to examine in vivo in the rat the possible impact of re-exposure to the context of a traumatic experience on the plasticity of the principle cells and on local circuit activity within the dentate gyrus (DG). Findings indicate that the re-exposure to a reminder of a traumatic experience affects not only aspects of synaptic plasticity of principle cells, but also aspects of local circuit activity. These alterations may underlie some of the behavioral consequences of the traumatic experience.
Neuroprotection in Multiple Sclerosis Translation of Experimental Therapy Results into Clinical Studies
Lecture
Wednesday, April 28, 2010
Hour: 14:30
Location:
Arthur and Rochelle Belfer Building for Biomedical Research
Neuroprotection in Multiple Sclerosis Translation of Experimental Therapy Results into Clinical Studies
Prof. Mathias Baehr
Head, Dept of Neurology
University of Gottingen Medical School, Germany
Experimental autoimmune encephalomyelitis (EAE) induced by myelin oligodendrocyte glycoprotein (MOG) in brown Norway rats mimicks neurodegenerative aspects of multiple sclerosis (MS). In this model, optic neuritis leads to acute axonal lesions and consecutive apoptotic cell death of RGCs, whose axons form the optic nerve. The intracellular mechanisms of RGC apoptosis resemble those described after surgical transection of the optic nerve. These mechanisms involve shifts in the expression of Bcl-2 family members, mitogen-activated protein kinases , and the phosphatidylinositol-3-kinase/Akt pathway.
Current research on neurodegenerative aspects in EAE or MS is focused on developing treatment strategies that inhibit degeneration of axons as well as protection of the neuronal cell body from apoptotic cell death. The concept of achieving neuroprotective effects by successful treatment of inflammation and autoimmunity was supported by studies showing a close association of axonal damage and inflammation. However, trials evaluating anti-inflammatory therapies in MS patients have shown that elimination of the inflammatory component of the disease does not necessarily stop progression of brain and spinal cord atrophy. Methylprednisolone, the standard treatment of autoimmune optic neuritis, accelerates visual recovery, but it does not influence the final visual outcome. In MOG-induced optic neuritis, even detrimental effects of anti-inflammatory treatment with methylprednisolone on the survival of RGCs were observed. On the other hand, blocking apoptosis signals in neurons without simultaneously treating inflammation-induced axon degeneration does not lead to functionally relevant results: Although application of Epo as well as CNTF increases survival rates of RGCs during MOG-induced optic neuritis, visual acuity in these animals remains poor due to severe and ongoing degeneration of optic nerve axon fibers. These observations led to a hypothesis that can easily be transferred to the situation in MS: Due to the much larger proportion of white matter in the human brain, preventing apoptosis of neuronal cell bodies alone might not find its expression in clinical scores and neurological function. Therefore, neuroprotective approaches in combination with the established disease-modifying therapies might be more promising. Simultaneous application of methylprednisolone and Epo or Minocycline in MOG-induced optic neuritis resulted in a functional, electrophysiological improvement of optic nerves and RGCs as well as in increased neuronal and axonal survival The lecture will outline the transfer of these experimental approaches into a clinical trial and discuss other new neuroprotective and regenerative strategies.
Habituation and adaptation in the barn owl
Lecture
Tuesday, April 27, 2010
Hour: 12:30
Location:
Jacob Ziskind Building
Habituation and adaptation in the barn owl
Dr. Yoram Gutfreund
Dept of Physiology and Biophysics
Faculty of Medicine, Technion, Haifa
Habituation is the most basic form of learning yet very little is known about the underlying mechanisms. In our lab, we use the pupil dilation reflex of the barn owl as a model system to study habituation. In barn owls the pupils dilate in response to an unexpected stimulus. This response habituates dramatically if the stimulus is repeated. The advantage of using the PDR is that it can be measured non-invasively in immobilized and even anaesthetized barn owls. This allows for an easy combination of physiological experiments with behavioral experiments. In my talk I will describe recent experiments addressing the effects of microstimulation in the optic tectum on the PDR and will show that neural responses in the optic tectum are correlated with the habituation of the PDR. These findings link the optic tectum with habituation processes.
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