Fall 2004 Seminar Series in Neuroscience

Tuesday Sept 14, 4-5 pm

Dr. Randy Ross, University of Colorado, Health Sciences Center

Title: Hypothesis: a prenatal nutritional supplement as a primary prevention strategy in schizophrenia

Abstract: The alpha7 nicotinic receptor gene alters early brain development, which alters physiological function, which changes attentional abilities, which is associated with risk for schizophrenia. From gene to disease, we will review the role of nicotinic mechanisms in schizophrenia and discuss the translation of this knowledge into a possible primary prevention strategy.

Tuesday Sept 28, 4-5 pm

Dr. Stuart Tobet, Department of Biomedical Sciences, Colorado State University

Title: Mammalian hypothalamus: Sex and development

Abstract: Steroid hormones dramatically influence the development of numerous sites in the nervous system. Basic mechanisms in neural development provide foci for understanding how factors related to sex can alter the ontogeny of these regions. Sex differences in neurogenesis, cell migration, cell differentiation, cell death, and synaptogenesis are being addressed. Any and all of these events serve as likely targets for genetic or gonadal steroid-dependent mechanisms throughout development. Although the majority of sexually dimorphic characteristics in brain have been described in older animals, many hormonal mechanisms that determine sexually differentiated brain characteristics occur during critical perinatal periods. It is likely that transient molecular events set the stage for later amplification by hormone actions. Sex differences in the positioning of cells in the developing hypothalamus further suggest that cell migration may be one key target for early gene actions that impact long-term susceptibility to brain sexual differentiation.

Tuesday Oct 12, 4-5 pm

Dr. Robert Sutherland (Canada)

Title: A behavioural analysis of the role of the hippocampus in long-term memory

Abstract:The idea that the hippocampus temporarily stores episodic memories until other regions of cortex form permanent memories has faced serious recent challenges. A series of experiments measuring retrograde amnesia after damage to the hippocampus shows that this view of memory is wrong and a reconceptualization will be presented based upon interactions between multiple long-term memory systems.

Week of Tuesday Oct 26

No Seminar Scheduled — Annual Society for Neuroscience Meeting, San Diego, CA

Tuesday Nov 2, 4-5 pm

Dr. Shu-Chan Hsu, Department of Cell Biology & Neuroscience, Rutgers University

Title: The role of exocyst complex in neuronal development

Abstract: A key initial step in the establishment of neuronal network is the outgrowth of neurites, a complex process that requires coordinated cytoskeleton remodeling and vesicle targeting to the plasma membrane. Recent work from my laboratory and from other labs suggests that the exocyst, a 734 kDa multisubunit protein complex, is essential for neurite outgrowth and regulation of vesicle trafficking in response to cellular signals. Based on this criterion, defining the function of the exocyst complex and using it as a molecular handle to identify other important components of the neurite outgrowth process has become the focus of my laboratory research. Three major approaches have been used to define the molecular mechanisms of exocyst function. First, we have generated highly specific antibodies to investigate correlations between endogenous exocyst distribution and outgrowth of neurites. Second, we characterized the molecular associations of the exocyst complex and their role in neurite outgrowth. Third, we set up in vitro protein binding/activity assays and in vivo transfection studies to determine the role of exocyst and its associated proteins in regulating neurite outgrowth. Based on our results we hypothesize that a role underlying exocyst’s function in promoting neurite outgrowth involves modulating cytoskeleton dynamics.

Tuesday Nov. 16, 4-5 pm

Dr. David Diamond, Department of Psychology, University of South Florida

Title: How does stress affect the hippocampal-prefrontal memory system

Abstract: The effects of stress on memory are complex. Intense stressful experiences, such as combat and assault, can produce memories that are so pathologically strong that they can interfere with the quality of life for people decades after the traumatic experience occurred. It is also a common occurrence that stress can cause people to be forgetful. How can stress enhance and also impair memory? This lecture will provide behavioral, pharmacological and molecular perspectives on stress-memory interactions, with a discussion of the involvement of the hippocampus, prefrontal cortex and amygdala in the modulation of memory by stress.

Tuesday Nov 30, 4-5 pm

No seminar scheduled on account of Front Range Neuroscience Group Meeting in Fort Collins.

Tuesday Dec 7, 4-5 pm

Dr. Jack Kinnamon, Department of Psychology, Denver University

Title: Rats with Good Taste

Abstract: The vertebrate taste bud is a dynamic system in which all of the cells are replaced approximately every 10 days to two weeks. During that time a given taste receptor cell matures, forms synaptic connections with sensory nerve fibers, performs its sensory functions, and then goes into senescence and dies. The taste bud is an amazing sensory organ. A typical mammalian taste bud contains approximately 100-150 cells, but is able to distinguish sweet, sour, salty, bitter and amino acids. While other sensory systems (e.g., auditory, olfactory, visual) use only one sensory transduction pathway, the gustatory system utilizes a variety of sensory transduction mechanisms. Gustatory receptor cells generate action potentials and convey the sensory information to the cranial nerves via chemical synapses. This is especially interesting because the gustatory receptor cells are epithelial and not neural in origin. My laboratory is studying how the taste receptor cells talk to the cranial nerves. We are especially interested in the synaptic proteins involved in the docking, fusion and exocytosis of synaptic vesicles.