Fall 2010 Seminar Series in Neuroscience

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

Tuesday Sept 14, 4-5 pm

Dr. Donal Skinner, Associate Professor, Department of Zoology and Physiology, University of Wyoming

Title:"Gonadotrophin-Releasing Hormone — the Reproductive Axis and Beyond"


Abstract: Gonadotrophin-releasing hormone (GnRH) is a hypothalamic decapeptide with an undisputed role as a primary regulator of reproduction. It exerts this regulation by controlling the release of the pituitary gonadotrophins. However, it is becoming apparent that GnRH may have a variety of other vital roles in normal physiology, which remains poorly understood. Reconsideration of the potential widespread action that is traditional reproductive hormone exerts may lead to the generation of novel therapies and provide insight into the seemingly incongruent outcomes from current treatments using GnRH analogues to combat diseases such prostate cancer.

Tuesday Sept 28, 4-5 pm

Dr. Philip Popovich, Professor, Department of Neuroscience, Ohio State University


Title: "Manipulating Innate Immunity to Promote Recovery After Spinal Cord Injury"


Abstract: Microglia and macrophages, collectively referred to as CNS mocrophages, are the predominant cells of innate immunity that influence outcome after traumatic or ischemic injury to the brain or spinal cord. These cells can be neurotoxic or support various indices of CNS repair. Understanding the mechanisms that regulate these divergent functions should lead to the development of novel therapeutics for various neurological disorders. In this presentation, data will be presented describing the complex regulation of CNS macrophages function along with prospects for controlling these cells to promote CNS repair.

Tuesday Oct 12, 4-5 pm

Dr. Kevin Jones, Associate Professor, Department of Molecular, Cellular, and Developmental Biology, University of Colorado at Boulder

Title: "Title TBA"


Abstract: Abstract TBA

Tuesday Oct 26, 4-5 pm

Dr. Boris Tabakoff, Professor, Department of Pharmacology, University of Colorado at Denver

Title: "Genetical/Genomics Reveal Why Animals (and Humans) Drink Alcohol"


Abstract: The consumption of Alcohol is an integral component of the behavior of approximately 70% of the American public. The levels of alcohol consumption are related to alcohol-related problems including accidents, violence, and alcohol dependence. In both non-human animals and humans, heritable factors play a role in one's predisposition to quantities of alcohol consumed on average. We used the genetical/genomics approach (Jensen, RC and Nap, IP, Trends Genetics 17:388 (2001))

Tuesday Nov, 9, 4-5 pm

Dr. Guido Frank, Assistant Professor, Department of Psychiatry, University of Colorado at Denver


Title: "Neuroimaging of Eating Disorders"


Abstract:The conceptual framework of the pathophysiology and etiology of the eating disorders (EDs) anorexia nervosa (AN), bulimia nervosa (BN) as well as emerging ED binge disorder (BED), has undergone significant changes in the past few decades. Brain imaging techniques now give us the opportunity to assess regional brain activity and neuroreceptor function in vivo in humans, and thus may help us understand how neuronal circuits are related to behavior and pathophysiology.
A host of neuroimaging tools are now available for ED research. Structural imaging techniques such as computer tomography (CT) and radiation-free magnetic resonance imaging (MRI) provide information on gross structural abnormalities. Magnetic resonance spectroscopy (MRS) can detect brain chemicals containing choline, aspartame and others, which are involved in brain neurotransmission. Positron emission tomography (PET), single photon emission computed tomography (SPECT) and functional magnetic resonance imaging (fMRI) are used to assess brain activity thought to be associated with changes in regional cerebral blood flow (rCBF). In addition, neurotransmitter receptor function and regional cerebral glucose metabolism (rCGM) can be assessed with PET and SPECT and radioligands. Electroencephalography (EEG) and evoked potentials (EPs) record neuronal electrical activity, and quantitative electroencephalography (qEEG) employs spectral analysis of EEG data from multiple-electrode, whole-head recordings and provides better spatial resolution compared to the traditional EEG. Recent advances in the field of brain research using neuroscience-based imaging paradigms have made great progress with respect to emotional and cognitive processes that may be altered in psychiatric illness. For example, a lot has been learned about brain pathways that are involved in fear provoked stimuli, cognitive flexibility, and numerous other areas with potentially direct relevance to eating disorders. In comparison with, for instance, psychosis or depression, the body of neurobiological research in EDs is relatively small, but nevertheless significant advances have been made over the past ten years to shed light on biologic brain processes that may be part of the pathophysiology of AN, BN, and BED.

Tuesday Dec 7, 4-5 pm

Dr. Todd Sacktor, Professor, Department of Physiology and Pharmacology, State University of New York Downstate Medical Center

Title: “PKMZ, LTP, Maintenance, and the Dynamic Molecular Biology of Memory Storage”


Abstract:How memories persist is a fundamental neurobiological question. The most commonly studied physiological model of memory is long-term potentiation (LTP). The molecular mechanisms of LTP can be divided into two phases: induction, triggering the potentiation; and maintenance, sustaining the potentiation over time. Although many molecules participate in induction, very few have been implicated in the mechanisms of molecules participate in induction, very few have been implicated in the mechanisms of maintenance participate in induction. Understanding maintenance, however, is critical for testing the hypothesis that LTP sustains memory storage in the brain. Only a single molecule has been found both necessary and sufficient for maintaining LTP — the brain-specific, atypical PKC isoforms, protein kinase Mzeta (PKMZ). Although full-length PKC isoforms respond to transient second messengers, and are involved in LTP induction, PKCZ is a second messenger-independent kinase, consisting of the independent catalytic domain of PKCZ, and is persistently active to sustain LTP maintenance. PKMZ is produced by a unique PKMZ mRNA, which is generated by an internal promoter within the PKC gene and transported to the dendrites of neurons. LTP induction increases new PKMZ synthesis, and the increased level of PKMZ then enhances synaptic transmission by doubling the number of post-synaptic AMPA receptors (AMPAR) through GluR2 subunit-mediated trafficking of the receptors to the synapse, PKMZ mediates synpatic potentiation specifically during the late-phase of LTP, as PKMZ inhibitors can reverse established LTP when applied several hours after tetanization in hippocampal slices or 1 day after tetanization in vivo. These studies set the stage for testing the hypothesis that the mechanism of LTP maintenance sustains memory storage. PKMZ inhibition in the hippocampus after learning eliminates the retention of spatial memory. Once the PKMZ inhibitor has been eliminated, the memory is still erased, but new spatial memories can be learned and stored. Similar results are found for conditioned taste aversion when the inhibitor is injected in the insular neocortex. Thus PKMZ is the first molecule found to be component of the long-term memory trace.