Dr. Margaret C. Biber
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Contact Information
Dr. Margaret C. Biber
Professor
Department of Physiology and Biophysics
Virginia Commonwealth University
P.O. Box 980551
Richmond, Virginia 23298-0551
Tel: 804-827-2221
Fax: 804-828-7382
email: mbiber@vcu.edu |
Margaret C. Biber completed her undergraduate degree in 1964 in Physiology at University College, London, her D.Phil. in 1967 in Biochemical Pharmacology at the University of Oxford, and then did two years of postdoctoral work in Neuropharmacology at Yale University. While at Yale she was the A.B. Coxe Memorial Fellow from 1967-1968. After serving on the faculty of the Yale University School of Medicine from 1969 -1975, she joined the Department in 1975 where she served as an Established Investigator of the American Heart Association from 1975-1980. She served as chair of the Department of Physiology from 1993 to 2007.
Teaching
In recent years, my teaching responsibilities have expanded and now involve lectures to graduate students and three groups of professional students (dental, pharmacy and medical) in a variety of areas that include cell physiology, cardiovascular physiology, neuroscience and selected topics in patho-physiology. In addition, I currently direct the graduate course on Cell Physiology (PHIS 604).
Research
My initial research focused on the regulation of norepinphrine synthesis in sympathetically innervated tissue, but later shifted to biochemical studies on regulation of the function of serotonin (5-hydroxytryptamine, 5-HT) neurons in the brain. The cell bodies of these neurons lying within the raphe nuclei, are few in number, but give rise to massively branching bilateral projections that supply the central nervous system (CNS). . Consistent with this organization, serotonin serves as a modulator in the CNS, influencing numerous functions such as motor activity, sensitivity to sensory inputs, pain, sleep and mood or affect. Compelling, albeit circumstantial, clinical evidence indicates that serotonin has a key role in mental health. For example, severe depression is associated with lowered CSF levels of the serotonin metabolite, 5-hydroxyindole acetic acid and depressive symptoms are exacerbated by manipulations that reduce 5-HT synthesis. Other evidence supporting serotonin’s involvement in depression is the efficacy of fluoxetine (Prozac), a highly selective serotonin reuptake inhibitor. Significantly, stress appears to be an important factor in triggering depression.
My colleagues and I developed an auditory stress model to activate the ascending 5-HT projections in brains of normal rats. Using this model, we identified a link between serotonergic neuronal activation, glucocorticords, and corticotropin releasing factor, all of which have been implicated in depression. We used this paradigm to probe both the neuronal and hormonal circuitry that mediates the response of the ascending serotonergic neurons with the aim of contributing to the understanding of the etiology of depression. These studies were supported by funding from the NIH (NINDS). At the present time, no training opportunities are available on this project.
Selected Publications
Daugherty, W.P., Corley, K.C., Phan, T-H., Boadle-Biber, M.C. Further studies on the activation of rat median raphe serotonergic neurons by inescapable sound stress. Brain Res. 923: 103-111, 2001 PubMed
Corley, K.C., Phan, T-H., Daugherty, W.P. and Boadle-Biber, M.C. Stress-induced activation of median raphe serotonergic neurons in rats is potentiated by the neurotensin antagonist, SR 48692. Neurosci. Lett. 319: 1-4, 2002 PubMed
Dilts, R.P., Novitzki, M., Phan, T-H., Corley, K.C., and Boadle-Biber, M. Neurotensin inhibits the activation of midbrain serotonergic neurons produced by random inescapable sound. Brain Research, 1996. PubMed
Dilts, R.P., and Boadle-Biber, M.C., Differential activation of the 5-hydroxytrytamine containing neurons of the midbrain raphe of the rat in response to randomly presented inescapable sound. Neurosci. Lett. 199: 78-80, 1995. PubMed
Singh, V.B., Kalimi, M., Phan, T-H, and Boadle-Biber, M.C., Intracranial Dehydroepiandrosterone Blocks the Activation of Trytophan Hydroxylase in Response to Acute Sound Stress. Mol. Cell. Neuroscience 5, 176-181, 1994
Boadle-Biber, M.C. Regulation of Serotonin Synthesis. Prog. Biophys. Molec. Biol. Vol.60:1-15, 1993. PubMed
Boadle-Biber, M.C., Singh, V.B., Corley, K.C., Phan, T-H., and Dilts, R.P. Evidence that Corticotropin-Releasing Factor within the Extended Amygdala Mediates the Activation of Tryptophan Hydrxylase Produced by Sound Stress in the Rat. Brain Res., 628:105-114, 1993. PubMed
Singh, V.B., Corley, K.C., Phan, T-H. and Boadle-Biber, M.C. Increases in the activity of tryptophan hydroxylase from rat cortex or midbrain in response to acute or repeated sound stress are blocked by adrenalectomy and restored by dexamethasone treatment. Brain Res., 516:66-76, 1990. PubMed
