In this section
Janice H. Urban, PhD
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, Dr. Urban 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 of 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 Discipline Chair of Physiology and Biophysics.
Silveira Villarroel H, Bompolaki M, Mackay JP, Miranda Tapia AP, Michaelson SD, Leitermann RJ, Marr RA, Urban JH, Colmers WF. NPY Induces Stress Resilience via Downregulation of I(h) in Principal Neurons of Rat Basolateral Amygdala. J Neurosci 38:4505-4520 (2018).
Blume SR, Freedberg M, Vantrease JE, Chan R, Padival M, Record MJ, DeJoseph MR, Urban JH, Rosenkranz JA. Sex- and Estrus-Dependent Differences in Rat Basolateral Amygdala. J Neurosci 37:10567-10586 (2017).
Jamnia N, Urban JH, Stutzmann GE, Chiren SG, Reisenbigler E, Marr R, Peterson DA, Kozlowski DA. A Clinically Relevant Closed-Head Model of Single and Repeat Concussive Injury in the Adult Rat Using a Controlled Cortical Impact Device. J Neurotrauma 34:1351-1363 (2016).
Leitermann RJ, Rostkowski AB, Urban JH. Neuropeptide Y input to the rat basolateral amygdala complex and modulation by conditioned fear. J Comp Neurol 524:2418-2439 (2016).
Woitowich NC, Philibert KD, Leitermann RJ, Wungjiranirun M, Urban JH, Glucksman MJ. EP24.15 as a Potential Regulator of Kisspeptin Within the Neuroendocrine Hypothalamus. Endocrinology 157:820-830 (2015).
Sladek CD, Michelini LC, Stachenfeld NS, Stern JE, Urban JH. Endocrine-Autonomic Linkages. Compr Physiol 5:1281-1323 (2015).
Dubois SL, Acosta-MartÃnez M, DeJoseph MR, Wolfe A, Radovick S, Boehm U, Urban JH, Levine JE. Positive, but not negative feedback actions of estradiol in adult female mice require estrogen receptor α in kisspeptin neurons. Endocrinology 156:1111-1120 (2014).
Taylor BK, Fu W, Kuphal KE, Stiller CO, Winter MK, Chen W, Corder GF, Urban JH, McCarson KE, Marvizon JC. Inflammation enhances Y1 receptor signaling, neuropeptide Y-mediated inhibition of hyperalgesia, and substance P release from primary afferent neurons. Neuroscience 256:178-194 (2013).
Rostkowski AB, Leitermann RJ, Urban JH. Differential activation of neuronal cell types in the basolateral amygdala by corticotropin releasing factor. Neuropeptides 47:273-280 (2013).
Sweis BM, Veverka KK, Dhillon ES, Urban JH, Lucas LR. Individual differences in the effects of chronic stress on memory: behavioral and neurochemical correlates of resiliency. Neuroscience 246:142-159 (2013).
Li X, DeJoseph MR, Urban JH, Bahi A, Dreyer JL, Meredith GE, Ford KA, Ferrario CR, Loweth JA, Wolf ME. Different roles of BDNF in nucleus accumbens core versus shell during the incubation of cue-induced cocaine craving and its long-term maintenance. J Neurosci 33:1130-1142 (2013).
Leitermann RJ, Sajdyk TJ, Urban JH. Cell-specific expression of calcineurin immunoreactivity within the rat basolateral amygdala complex and colocalization with the neuropeptide Y Y1 receptor. J Chem Neuroanat 45:50-56 (2012).
Geisbrecht C, Mackay J, Silveira H, Urban JH, Colmers WF. Countervailing modulation of Ih by neuropeptide Y and corticotrophin-releasing factor in basolateral amygdala as a possible mechanism for their effects on stress-related behaviors. J Neurosci 30:16970-16982 (2010).
Rostkowski AB, Teppen TL, Peterson DA, Urban JH. cell-specific expression of Neuropeptide Y Y1 receptor immunoreactivity in the rat basolateral amygdala. J Comp Neurol 16:166-176 (2009).
Sajdyk TJ, Johnson PL, Leitermann RJ, Fitz SD, Dietrich A, Morin M, Gehlert DR, Urban JH, Shekhar A. Neuropeptide Y (NPY)-mediated behavioral plasticity in the amygdala induces stress resilience. J Neurosci 28: 893-903 (2008).
Dimitrov ED, DeJoseph MR, Brownfield MS, Urban JH. Involvement of neuropeptide Y Y1 receptors in the regulation of neuroendocrine corticotropin releasing hormone neuronal activity. Endocrinology 148:3666-3673 (2007).
Taylor BK, Abhyankar SS, Vo, NT, Kreidt CL, Churi SB, Urban JH. Neuropeptide Y acts at Y1 receptors in the rostral ventral medulla to inhibit neuropathic pain. Pain: 131:83-95 (2007).
Urban JH, Leitermann R, DeJoseph MR, Somponpun SJ, Wolak ML, Sladek CD. Influence of dehydration on the expression of neuropeptide Y Y1 receptors in hypothalamic magnocellular neurons. Endocrinology 147:4122-4131 (2006).
Thomas R, Urban JH, Peterson DA. Acute exposure to predator odor elevates corticosterone without altering proliferation in the adult rat dentate gyrus. Exp Neurology 201: 308-315 (2006).
Hill JW, Urban JH, Xu M, Levine JE. Estrogen induces neuropeptide Y Y1 receptor gene expression and responsiveness to NPY in gonadotrope-enriched pituitary cell cultures. Endocrinology 145:2283-90 (2004).
Wolak ML, deJoseph MR, Brownfield MS, Urban JH. Distribution of neuropeptide Y Y1 and Y5 receptors in the rat brain using immunohistochemistry. J Comp Neurol 464:285‑311 (2003).
Mortimer JE, Urban JH. Long-term toxicities of selective estrogen-receptor modulators and antiaromatase agents. Oncology 17:652‑9 (2003).
Xu M, Urban JH, Hill JW, Levine JE. Regulation of hypothalamic neuropeptide Y Y1 receptor gene expression during the estrous cycle: role of progesterone receptors. Endocrinology 141:3319-3327 (2000).
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.
|From the left Randy Leitermann, Amanda Rostkowski, Dr. Urban, and Bill Chura (Lab Neuroscience 2006)|