Spring 2008 Seminar Series in Neuroscience

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


Tuesday Jan 29, 4-5 pm	Dr. Paul Durham, Department of Biology, Missouri State University, Springfield MO TITLE: “Increased Neuronal-Satellite Glial Cell Signaling in Trigeminal Ganglion in Response to Trigeminal Nerve Activation: Implications for Migraine and Temporomandibular Joint (TMJ) Disorders“ Abstract: Activation of trigeminal ganglion nerves is implicated in the pathology of migraine and temporomandibular joint (TMJ) disorders. Cell bodies of trigeminal neurons reside in the ganglion in close association with satellite glial cells. Neuron-glia interactions via gap junctions and paracrine signaling are thought to be involved in all stages of inflammation and pain associated with several CNS diseases. However, the role of neuron-glia communication within the trigeminal ganglion under normal and inflammatory conditions is not known. Based on recent studies, we now have evidence of increased neuron-satellite glial cell signaling via gap junctions within the trigeminal ganglion in response to trigeminal nerve activation. We also have shown that the neuropeptide calcitonin gene-related peptide can increase the level of iNOS and the production of nitric oxide from satellite glial cells. Based on our findings, it is likely that neuronal-glial communication via gap junctions and paracrine signaling are involved in the development of peripheral sensitization within the trigeminal ganglion and, thus, are likely to play an important role in migraine and TMJ pathologies. Furthermore, we propose that propagation of inflammatory signals within the ganglion may help to explain commonly reported symptoms of comorbid conditions associated with migraine and TMJ pathology.
Tuesday Feb 19, 4-5 pm	Dr. Anu Sharma, Department of Speech, Language and Hearing Studies, Institute for Cognitive Sciences, University of Colorado at Boulder and Department of Otolaryngology at UCHSC TITLE: " Critical Periods for cortical development and re-organization in deaf children who are fitted with cochlear implants" Abstract: We are investigating the deterioration, development, plasticity and re-organization of the human central auditory pathways in normal hearing children and in deaf children who regain hearing after being fitted with cochlear implants. Our measures of central auditory maturation include cortical auditory evoked potentials (CAEP), high density electroencephalography (EEG), Magnetoencephalography (MEG) and behavioral measures. We will discuss results using these and other brain imaging measures in humans and in animal models of deafness. In a series of experiments we have established the existence of and time limits of a critical period for development of the central auditory pathways. If stimulation is delivered within that period of 3.5 years, CAEP latencies reach age-normal values within months following the onset of stimulation. However, if stimulation is withheld for more than 7 years, we find reduced plasticity as evidenced by abnormal CAEP responses. This lack of central auditory development in congenitally deafened late-implanted children is correlated with relatively poor development of speech and language skills. Animal models suggest that primary auditory cortex may be functionally decoupled from higher-order auditory cortex, due to restricted development of inter- and intra- cortical connections, in congenitally cats and children who have been deaf for long periods of time. Another aspect of plasticity that works against late-implanted children is the re-organization of higher order cortex by other sensory modalities (e.g.,vision, somatosensation). The hypothesis of cortical re-organization in children deprived of sound for a long time provides an account for the oral language-learning difficulties of children who receive a cochlear implant after the end of the critical period.
Tuesday Mar 4, 4-5 pm	Dr. Robert Dantzer, Professor of Psychoneuroimmunology at the Department of Pathology and Department of Animal Sciences of the University of Illinois at Urbana-Champaign TITLE: “From inflammation to sickness and depression: When the immune system subjugates the brain” Abstract: In response to a peripheral infection, innate immune cells produce proinflammatory cytokines that act on the brain to cause sickness behaviour. When activation of the peripheral immune system continues unabated, such as during systemic infections, cancer and autoimmune diseases, the ensuing immune signalling to the brain can lead to exacerbation of sickness and development of symptoms of depression in vulnerable individuals. These phenomena may account for the increased prevalence of clinical depression in physically ill people. Inflammation is an important biological event that increases the risk of major depressive episodes, much like the more traditional psychosocial factors.
Tuesday March 18, 4-5 pm	Dr. Barry E. Levin, Neurology Service, VA Medicial Center and Department of Neurosciences; University of Medicine and Dentistry of New Jersey, New Jersey Medical School TITLE: “Exercise and obesity: it’s mostly in your brain” Abstract: There is an obesity epidemic among children and adults in the U.S. Unfortunately, more that 90% of obese subjects regain lost weight after dieting. Exercise appears to be an important adjunct in those few individuals who succeed at losing and keeping off weight for more than 2 years. For this reason, we have studied the interactions of obesity, genotype, age and diet on the efficacy of exercise in lowering body weight and adiposity in rats selectively bred to develop diet-induced obesity (DIO) on a moderate (31%) fat diet. Exercise lowers body weight, adiposity and leptin levels in DIO rats. The lowered leptin levels should alter central pathways to trigger increased food intake but exercising DIO rats do not compensate for lost weight by eating more and their brain regulatory systems do not differ from sedentary rats. However, when exercise ceases, adult DIO rats quickly regain lost weight, even on low fat diets. On the other hand, when weanling DIO rats are placed on a 31% fat diet and given a running wheel for only 3 weeks, they fail to become obese during exercise and for at least 10 weeks after exercise cessation. This sustained resistance to the development of obesity is associated with increased central sensitivity to negative feedback signals from leptin and with persistent alterations in central regulatory pathways. Thus, the brain is a critical regulator of energy homeostasis and exercise provides some signals which encourage weight loss in adult rats and favorably alter the development central regulatory pathways to prevent weight regain after exercise cessation in juvenile rats. Such findings may have important implications for prevention of childhood obesity.
Tuesday April 8, 4-5 pm	Dr. Monika Fleshner, Department of Integrative Physiology, University of Colorado at Boulder TITLE: “Extracellular Hsp72: A Double-Edged Sword for Health” Abstract: Environmental or emotional challenge triggers a cascading series of physiological responses that are collectively termed the “stress response”. The stress response can be assessed at the behavioral, neural, hormonal, immunological and single cell, levels and evolved to benefit an organism’s chance of survival during times of acute challenge. The stress response has been studied for many years, however, its impact on specifically immune function has only recently been appreciated. Acute activation of the stress response has both inhibitory and stimulatory effects on immunity. The focus of this presentation is on a novel mechanism for the immunostimulatory effects of stress. Specifically, we propose that an endogenous, ubiquitous cellular stress protein, heat shock protein 72, when found in the extracellular environment may contribute to stress-induced potentiation of innate immunity. We develop the hypothesis that the release of extracellular heat shock protein 72 (eHsp72) is a normal feature of the acute stress response that can have either positive or negative consequences for host defense depending on several factors, including the nature of the eHsp72 (naked versus antigen-associated), and host health status (absence or presence of pre-existing inflammatory disease). Thus, stress-induced eHsp72 release may be a double-edged sword for host defense.
Tentatively: Tuesday April 15, 4-5 pm	Dr. James Bamburg, Professor, Department of Biochemistry and Director of the Molecular, Cellular and Integrative Neuroscience Program, Colorado State University, Fort Collins, CO TITLE: “Wiring and unwiring the brain: ADF/cofilin in growth cone pathfinding and neurodegeneration” Abstract: Actin filaments (F-actin) constitute a dynamic component of the cytoskeleton of eukaryotic cells. Processes of cellular motility and cell division are dependent upon a pool of actin subunits capable of rapid assembly and disassembly in response to extracellular signals. The interaction of actin with the cell membrane and the spatial and temporal changes in actin organization which underlie cell movement and neuronal pathfinding are largely regulated by a number of actin binding proteins, among the most important of which is actin depolymerizing factor (ADF) and its related family member, cofilin. ADF and cofilin (AC) are essential 18.5 kDa proteins first isolated from brain. All eukaryotic organisms including plants and protists have an AC protein. Immunofluorescence localization of AC showed it to be particularly enriched in the leading edge of cultured fibroblasts and in neuronal growth cones. AC is spatially and temporally localized with actin. Both in vitro and in vivo, AC serves to rapidly increase actin filament dynamics. Silencing AC activity inhibits cellular processes dependent upon actin reorganization. AC activity is regulated by several mechanisms, including phosphorylation of a single serine residue. Since transmembrane signaling culminates in changes in the activity of protein kinases or phosphatases, AC is a key protein through which extracellular ligands bring about an alteration in cytoskeletal organization, the key to growth cone pathfinding. However, AC is rapidly dephosphorylated in response to neuronal stress. AC overactivation results in the formation of cytoplasmic rods containing actin and AC. Rods block axonal transport and cause loss of synaptic function. Rods and other cofilin inclusions are found in Alzheimer’s disease brain.
Tuesday April 29, 4-5 pm	Dr. Rusiko Bourchaladze TITLE: "cAMP and Memory: From Genes to Development of Drugs to Treat Cognitive Disorders" Abstract: In this talk, I will discuss: (i) the role of cAMP signaling on plasticity , learning and memory; (ii) the novel neurogenetic and neuropharmacalogical approaches to discover genes important for memory; and (iii) the development of drugs to treat cognitive disorders.