Spring 2009 Seminar Series in Neuroscience

Location of Seminars: Muenzinger E214 (See map and directions)

Tuesday Feb 3, 4-5 pm

Dr. Michael Oshinsky, Department of Neurology, Thomas Jefferson University Medical College

TITLE: “Modeling the Chronification of Headache“

Abstract: In this talk, we will discuss the development and features of an animal model of chronic daily headache. Chronic daily headache (CDH) is a neurological disorder characterized by > 15 headache days per month and affects up to 4% of the general population! Most cases of CDH evolve from episodic migraine. CDH patients experience chronic cranial tenderness (allodynia) with episodes of increased headache pain. Little is known about how episodic headache progresses and transforms into CDH. Of course, we start off the discussion by answering the most important question: How do you know if a rat has a headache?

Tuesday Feb 17, 4-5 pm Dr. Morris Moscovitch, Max and Gianna Glassman Chair in Neuropsychology and Aging, Department of Psychology, University of Toronto

TITLE: " The Hippocampus As a “Stupid,” Domain-Specific Module: Implications for Theories of Recent and Remote Memory, and of Imagination"

Abstract: The hippocampus and surrounding regions of the medial temporal lobe play a central role in all neuropsychological theories of memory. It is still a matter of debate, however, how best to characterize the functions of these regions, the hippocampus in particular. In this article, I examine the proposal that the hippocampus is a “stupid” module whose specific domain is to consciously apprehend information. A number of interesting consequences for the organization of memory and the brain follow from this proposal and the assumptions it entails. These, in turn, have important implications for neuropsychological theories of recent and remote episodic, semantic, and spatial memory and for the functions that episodic memory may serve in perception, comprehension, planning, imagination, and problem solving. I consider these implications by selectively reviewing the literature and primarily drawing on research my collaborators and I have conducted.
Tuesday Mar 3, 4-5 pm

Dr. Peter Kalivas, Professor and Chair, Department of Neurosciences, Medical University of South Carolina, Charleston, SC.

TITLE: “Giving Addicts a Choice by Restoring Excitatory Neuroplasticity”

Abstract: Using addictive drugs can evolve from controlled social use into the compulsive relapsing disorder that characterizes addiction. This transition to addiction results from genetic, developmental, and sociological vulnerabilities, combined with pharmacologically induced plasticity in brain circuitry that strengthens learned drug-associated behaviors at the expense of adaptive responding for natural rewards. Advances over the last decade have identified the brain circuits most vulnerable to drug-induced changes, as well as many associated molecular and morphological underpinnings. This growing knowledge has contributed to an expanded understanding of how drugs usurp normal learning circuitry to create the pathology of addiction, as evidenced by involuntary activation of reward circuits in response to drug-associated cues and simultaneous reports of drug craving. This new understanding provides unprecedented opportunities for novel pharmacotherapeutic targets in treating addiction. There appears to be plasticity associated with the addiction drugs. These findings also provide the basis for the current understanding of addiction as a chronic, relapsing disease of the brain with changes that persist long after the last use of the drug. Here, we describe the neuroplasticity in brain circuits and cell function induced by addictive drugs that is thought to underlie the compulsions to resume drug-taking, and discuss how this knowledge is impelling exploration and testing of novel addiction therapies.

Tuesday March 17, 4-5 pm

Dr. Erik Willcutt, Department of Psychology, University of Colorado at Boulder

TITLE: “Using Neuroscience and Genetics to Understand the “Whirling Ball of Comorbidity”: ADHD, Learning Disabilities, and Related Disorders.”

Abstract: Until recently most cognitive models of mental disorders suggested that each disorder resulted from a single core neurocognitive deficit that was caused by a specific genetic or environmental risk factor. However, these single-deficit theories are challenged by the frequent comorbidity, or co-occurrence, of two or more different disorders in the same individual. This presentation will describe clinical, neuropsychological, and genetic approaches that we have used to test competing explanations for comorbidity between reading disability (RD) and attention-deficit/hyperactivity disorder (ADHD). Results from our study and others suggest that RD and ADHD are each influenced by at least ten different genes, and subset of these genes increase risk for both disorders. Contrary to the predictions of single-deficit models, neuropsychological analyses suggest that these shared genetic influences lead to significant weaknesses in working memory, cognitive speed, and sustained attention in both disorders. In contrast, RD is uniquely associated with deficits in phonological decoding, whereas ADHD is more strongly associated with poor inhibitory control.
Rather than a nuisance variable or an indicator of a flawed diagnostic system, comorbidity may be a useful tool to dissect the relations between complex disorders. A better understanding of the boundaries between diagnoses and the causes of comorbidity will help to refine the diagnostic nosology of psychological disorders in DSM-V and beyond.

Tuesday April 8, 4-5 pm

Dr. Gyorgy Buzsaki, Center for Molecular and Behavioral Neuroscience, Rutgers University

TITLE: “Internally Generated Cell Assembly Sequences In the Services of Cognition”

Abstract: A long-standing conjecture is that aspects of cognition depend on the brain’s ability to self-generate sequential neuronal activity. We found that reliably and continually changing cell assemblies in the rat hippocampus appeared not only during spatial navigation but also in the absence of changing environmental or body-derived inputs. During the delay period of memory task, each moment in time was characterized by the activity of a particular assembly of neurons. Identical initial conditions triggered a similar assembly sequence, whereas different conditions gave rise to different sequences, thereby predicting behavioral choices, including errors. Such sequences were not formed in control (nonmemory) tasks. We hypothesis that neuronal representations, evolved for encoding distance in spatial navigation, also support episodic recall and the planning of action sequences.

Tuesday April 21, 4-5 pm

Dr. Albert Kim, Institute of Cognitive Science, University of Colorado at Boulder