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Janice H Urban, PhD

Professor and Chair

Dr. Urban graduated from Saint Mary’s College, Notre Dame, Indiana with a degree in Biology and Chemistry. She completed her PhD thesis work in the Department of Pharmacology and Experimental Therapeutics at Loyola University Stritch School of Medicine where her work focused on the serotonergic regulation of stress hormone secretion. Afterwards, Janice pursued postdoctoral work in the Department of Pharmacology at the University of Washington in Seattle, WA examining the regulation of neuropeptides in limbic brain regions by gonadal steroids. Dr. Urban continued postdoctoral research in the Department of Neurobiology and Physiology at Northwestern University, and was a member of the Center for Reproductive Sciences at Northwestern University, Evanston, IL prior to joining the faculty in the Department of Physiology and Biophysics at the Chicago Medical School. Dr. Urban has an active research program in the areas of neuroendocrinology and elucidating mechanisms underlying stress resilience. She is active in graduate and medical teaching and is a member of the Society for Neuroscience, American Physiological Society, Endocrine Society and American Neuroendocrine Society. Dr. Urban is currently Professor and Chair of the department of Physiology and Biophysics.

Publications

Recent Publications

Xu M., Urban J.H., Hill J.W., Levine J.E.: Regulation of hypothalamic neuropeptide Y Y1 receptor gene expression during the estrous cycle: role of progesterone receptors. Endocrinology 141:3319-3327 (2000).

Mortimer J.E., Urban J.H.: Comparison of longterm toxicities associated with SERMS and inhibitors of aromatase. Oncology 17(5):652‑9 (2003).

Wolak M.L., deJoseph M.R., Brownfield M.S., Urban J.H.: Distribution of neuropeptide Y Y1 and Y5 receptors in the rat brain using immunohistochemistry. J Comp Neurol 464(3):285‑311 (2003).

Hill J.W., Urban J.H., Xu M., Levine J.E.: Estrogen induces neuropeptide Y Y1 receptor gene expression and responsiveness to NPY in gonadotrope-enriched pituitary cell cultures. Endocrinology 145:2283-90 (2004).

Thomas R., Urban J.H., Peterson D.A.: Acute exposure to predator odor elevates corticosterone without altering proliferation in the adult rat dentate gyrus. Exp Neurology 201: 308-315 (2006).

Urban J.H., Leitermann R., DeJoseph M.R., Somponpun S.J., Wolak M.L., Sladek C.D.: Influence of dehydration on the expression of neuropeptide Y Y1 receptors in hypothalamic magnocellular neurons. Endocrinology 147:4122-4131 (2006).

Taylor B.K., Abhyankar S.S., Vo, N.T., Kreidt C.L., Churi S.B., Urban J.H.: Neuropeptide Y acts at Y1 receptors in the rostral ventral medulla to inhibit neuropathic pain. Pain: 131:83-95 (2007).

Dimitrov E.D., DeJoseph M.R., Brownfield M.S., Urban J.H.: Involvement of neuropeptide Y Y1 receptors in the regulation of neuroendocrine corticotropin releasing hormone neuronal activity. Endocrinology 148:3666-3673 (2007).

Sajdyk T.J., Johnson P.L., Leitermann R.J., Fitz S.D., Dietrich A., Morin M., Gehlert D.R., Urban J.H., Shekhar A.: Neuropeptide Y (NPY)-mediated behavioral plasticity in the amygdala induces stress resilience. J Neuroscience 28: 893-903 (2008).

Rostkowski A.B., Teppen T.L., Peterson D.A., Urban J.H.: cell-specific expression of Neuropeptide Y Y1 receptor immunoreactivity in the rat basolateral amygdala. J Comp Neurol 16:166-176 (2009).

Geisbrecht C., Mackay J., Silveira H., Urban J.H., Colmers W.F.: Counterveiling modulation of Ih by NPY and CRF in basolateral amygdala as a possible mechanism for the effects on stress-related behaviors. J Neuroscience: in press (2010).

Research Projects

Neuropeptide Y, NPY receptors, neuroendocrine function,stress, sex differences

Stress is a major causal factor in the etiology of a number of psychiatric-related disorders. However, some individuals remain stress resilient and persevere in the face of intense stress. The mechanisms contributing to stress resistance, or resilience, are beginning to come to light. Numerous studies indicate that NPY is clearly an endogenous anxiolytic (stress reducing or buffering) compound within the amygdala, and its association with resilience in humans has been demonstrated in various studies since the 1980s. Our research is focused on understanding the contribution of neuropeptide systems, such as NPY within the hypothalamus and amygdala, to modulating behavioral and endocrine responses to stress.

The focus of this research is to elucidate the pathways and mechanisms in the brain involved in the generation of stress resilience which will be useful for preventive and therapeutic treatment of anxiety-related disorders. The basolateral nucleus of the amygdala (BLA) is one brain region that is essential for the integration and processing of sensory and memory information into stress responses and emotion. BLA activity is reflective of the balance of inhibitory and excitatory tone which is modulated, in part, by neuropeptide Y (NPY) and corticotrophin-releasing factor (CRF), respectively. In the BLA, NPY not only buffers the actions of CRF, but produces long term stress resilience likely through decreasing the output of the BLA. Recent studies demonstrate that NPY and CRF receptors, present on glutamatergic cells in the BLA, exert opposing physiological actions on their excitability. That both of these peptides are present on these glutamatergic cells makes them a nexus for the two different stress signals in modulating the output of the BLA which contributes to the emotional behaviors of the individual.

 

Another aspect of our research is to understand the contribution of neuropeptide systems within the hypothalamus (NPY, oxytocin, CRF) to modulating stress responses. Current projects in the laboratory focus on identifying the distribution of NPY receptors within stress responsive areas (such as the paraventricular nucleus of the hypothalamus and central amygdala) and the extent to which these receptors contribute to neuroendocrine function. Along these lines, we have demonstrated sex differences in the neuroendocrine responses to stress and estrogenic regulation of NPY receptor expression and actions in females. The steroid modulation of NPY systems may contribute to the sex differences observed in stress responses.

Lab Members

Lab Neuroscience 2006
From the left Randy Leitermann, Amanda Rostkowski, Dr. Urban, and Bill Chura (Lab Neuroscience 2006)