S. Wood

Susan K. Wood, Ph.D.
Assistant Professor
Training:
Postdoctoral
Children’s Hospital of Philadelphia/Univ of Pennsylvania
Michigan State Univ
Ph.D.: University of Michigan
B.S.: University of Michigan
Contact Information:
Phone: 803-216-3522
Fax: 803-216-3549
E-mail: susan.wood@uscmed.sc.edu
Web Page

Research Focus:

Chronic exposure to social stress leads to psychological disorders, such as depression, and increases cardiovascular disease risk in susceptible individuals. While the relationship between depression and cardiovascular disease is well recognized, central mechanisms underlying this comorbidity are unclear.  My laboratory uses a multidisciplinary approach that includes behavioral, cardiovascular, molecular biology, and electrophysiological techniques to identify the pathophysiology conferring vulnerability or resiliency to stress-related disease. By studying key brain regions implicated in depression and cardiovascular responses, such as the locus coeruleus (LC), the research in my lab aims to characterize novel targets or biomarkers of these stress-related pathologies. My previous work using a rodent model of social stress led to the discovery that corticotropin-releasing factor (CRF), a neurohormone that stimulates the behavioral, neuroendocrine, and cardiovascular stress response, plays a vital role in rendering an individual vulnerable to stress-induced depression and cardiovascular disease. As CRF serves as a neurotransmitter to modulate the activity of the LC-norepinephrine system ongoing studies in the lab will identify how enduring changes within this system contribute to depression-cardiovascular disease comorbidity.

Fluorescent photomicrograph of the locus coeruleus immunolabeled for tyrosine hydroxylase (green) and CRF (red).  This figure depicts the homogeneity of noradrenergic LC neurons (LC-NE).  The central nucleus of the amygdala is the major source of CRF terminating in the rostrolateral LC.  CRF afferents to the LC are one mechanism by which stress activates the LC-NE system. Under conditions of chronic LC activation, this mechanism is proposed to lead to pathology.

Recent Publications

PubMed link

Wood SK, McFadden K, Griffin T, Wolfe JH, Zderic SA, Valentino RJ. (2013) A corticotropin-releasing factor receptor antagonist improves urodynamic dysfunction produced by social stress or partial bladder outlet obstruction in rats. American Journal of Physiology: Regulatory Integrative and Comparative Physiology. (epub) in press.

Wood SK, Zhang XY, Reyes BA, Lee CS, Van Bockstaele EJ, Valentino RJ. (2013) Cellular adaptations of dorsal raphe serotonin neurons associated with the development of active coping in response to social stress. Biological Psychiatry. (epub) in press.

Wood SK, McFadden KV, Grigoriadis D, Bhatnagar S, Valentino RJ. (2012) Depressive and cardiovascular disease comorbidity in a rat model of social stress: A putative role for corticotropin-releasing factor. Psychopharmacology. 222(2): 325-336.

Valentino RJ, Wood SK, Wein A, Zderic S. (2011) The Bladder-Brain Connection: Evidence for a Role of Corticotropin-Releasing Factor. Nature Reviews Urology. 8(1): 19-28.

Wood SK, Walker HE, Valentino RJ, Bhatnagar S. (2010) Individual differences in reactivity to social stress predict susceptibility and resilience to a depressive phenotype: role of corticotropin-releasing factor. Endocrinology 151(4): 1795-1805. Highlighted in Endocrine News, March 2010.

Wood SK, Baez MA, Bhatnagar S, Valentino RJ (2009). Social stress-induced bladder dysfunction: potential role of corticotropin-releasing factor. The American Journal of Physiology: Regulatory, Integrative and Comparative Physiology 296(5): R1671-8.