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Robert J. Handa, PhDProfessor, Department of Basic Medical Sciences
UA Office Phone: (602) 827-2161 |
Education:Post Doc: Neuroendocrinology; Oregon Health Sciences University; 1984-1987 PhD; University of California, Los Angeles; 1984 MS; University of Arizona; 1979 Background:Dr. Handa received his Ph.D. from UCLA and then spent 3 years as a postdoctoral fellow at the Oregon Regional Primate Research Center and the Oregon Health Sciences University. He was a faculty member at Loyola University of Chicago Stritch School of Medicine and then at Colorado State University College of Veterinary Medicine prior to moving his laboratory to the University of Arizona College of Medicine - Phoenix in 2008. While at Stritch School of Medicine he served as Director of the Graduate Program in Molecular Biology and at Colorado State University he served as Associate Head for the Department of Biomedical Sciences and as the interim Director of the Molecular, Cellular and Integrative Neuroscience Graduate Program. His current teaching assignment at UACOM-P is in Clinical Anatomy Research Interests:Sex differences in the morphology and function of the central nervous system arise as a consequence of exposure to the gonadal steroid hormones, estradiol and testosterone, during development and adulthood. The actions of these steroid hormones are mediated via a family of intracellular receptors. Current research in the Handa laboratory is examining the molecular mechanisms of androgen and estrogen receptor action and the neurobiological and neuroendocrine systems modulated by these receptors. Our data show that these hormones regulate the neuroendocrine response (hormone secretion and neuropeptide synthesis) to physical and psychological stressors. The beta form of estrogen receptor, which is present in brain regions functionally relevant to neuroendocrine and autonomic regulation may provide insight into the mechanisms by which steroid hormones regulate stress responses. Indeed, our studies show that 3beta-Diol, a metabolite of the potent androgen, didhydrotestosterone, can act through estrogen receptor beta to inhibit the hormonal response to stressors, whereas estradiol acts through estrogen receptor alpha to augment the responses. The results of these studies provide a cellular mechanism to support the reported sex differences in stress hormone secretion and the dysregulation in the control of stress hormone secretion which accompanies behavior disorders such as depression. Our studies are also attempting to define the varied strategies adopted by males and females to cope with stressors which can deleteriously affect physiology. Developmental exposure to stress, glucocorticoids and neurotoxic agents can also influence the hormonal and behavioral responses to stress in adulthood. The mechanism whereby permanent changes in neuroendocrine function and behavior are altered by fetal insults is currently unknown. Our studies have examined the effects of prenatal stress, prenatal exposure to glucocorticoids and prenatal exposure to ethanol on the development of the hypothalamus. Our current studies are determining whether there are changes in expression of cell death genes, neuropeptide genes or neurotrophic factor genes in specific neuronal phenotypes following prenatal insults. Moreover, we are interested in knowing how these changes might alter anxiety-like and depressive-like behaviors in a sex-specific fashion. Ultimately, the results of these studies may be important in defining the fetal antecedents of adult neurobehavioral disorders. Gonadal steroid hormone receptors are well-known intracellular transcription factors. These hormones have powerful and widespread influences throughout the brain and ultimately, the actions of gonadal steroids must be examined in context of known neural circuits and neuroendocrine regulators. Our studies are aimed at determining some of the mechanisms underlying age-, development- and sex-related differences in the cellular and behavioral responses to intracellular and environmental signals and cues. Selected Publications:
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