Physiology

SEAN D. STOCKER, Ph.D. Assistant Professor Ph.D. University of Pittsburgh, 2002 Office: MS-611 Medical Center 0298 Tel: (859) 323-4344 Lab: MS-641 Tel: (859) 323-8762 E-mail: sdstoc3@uky.edu Curriculum Vita (pdf)

Our laboratory is a bridge between the cardiovascular and neurobiology fields. We employ several “state-of-the-art” neuroscience techniques to investigate how the central nervous system contributes to cardiovascular disease (hypertension, congestive heart failure). Project 1 focuses on the role of the central nervous system in obesity-induced hypertension. Recent clinical studies suggest that almost 2/3 of hypertension in men and women is attributed to obesity. Evidence from both humans and animals suggest that this obesity-induced hypertension is largely attributed to activation of regions and pathways in the brain to increase blood pressure. A major goal of our laboratory is to identify the central neural circuitry and cellular mechanisms that regulate blood pressure and understand how these pathways have changed in obesity-induced hypertension. Project 2 focuses on how changes in dietary salt contribute to the pathogenesis of salt-sensitive hypertension. Compelling evidence indicates that dietary salt intake influences the level of arterial blood pressure, in part, by changing the regulatory networks in the brain that regulate blood pressure. A major goal of our laboratory is to identify the cellular mechanisms that permit the brain to monitor the amount of salt in our bodies and determine how activation of these cellular mechanisms leads to changes in blood pressure. Ongoing studies in both projects utilize a variety of approaches including in vivo and in vitro electrophysiology, pharmacological manipulation of neurotransmission, neurophysiological recordings of sympathetic nerves, functional neuroanatomy, and genetic models of obesity and salt-sensitive hypertension.

Recent Publications:

Taylor AC, McCarthy JJ, STOCKER SD. Mice lacking the transient receptor receptor vanilloid-1 (TRPV1) channel display normal thirst responses and central Fos activation to hypernatremia. Am J Physiol Regul Integr Comp Physiol, 294(4): R1285-1293, 2008.

STOCKER SD, Osborn JL, Carmichael SP. Forebrain osmotic regulation of the sympathetic nervous system. Clin Exp Pharm Physiol, 35: 695-700, 2008.

Shi P, STOCKER SD, Toney GM. Organum vasculosum laminae terminalis (OVLT) contributes to increased sympathetic nerve activity induced by central hyperosmolality. Am J Physiol Regul Integr Comp Physiol, 293(6): R2279-R2289, 2007.

Adams JM, Madden CJ, Sved AF, and STOCKER SD. Increased dietary salt enhances both sympathoexcitatory and sympathoinhibitory responses evoked from the rostral ventrolateral medulla. Hypertension, 50(2): 354-359, 2007.

STOCKER SD, Meador R, and Adams JM. Neurons of the rostral ventrolateral medulla contribute to diet-induced obesity hypertension in rats. Hypertension, 49(3): 640-646, 2007.

Madden CJ, STOCKER SD, and Sved AF. Homeostatic responses to hypotension and glucodeprivation are attenuated following selective destruction of the C1-catecholaminergic cell population of the rostral ventrolateral medulla (RVLM) in rats. Am J Physiol Regul Integr Comp Physiol , 291(3):R751-R759, 2006.

STOCKER SD and Toney GM. Vagal afferent input alters the discharge of osmotic and ANG II-responsive median preoptic neurons projecting to the hypothalamic paraventricular nucleus. Brain Research, 1131(1): 118-128, 2007

STOCKER SD, Wilson ME, Madden CJ, Lone U, and Sved AF. Intravenous 6-hydroxydopamine attenuates vasopressin and oxytocin secretion stimulated by hemorrhage and hypotension but not hyperosmolality. Am J Physiol Regul Integr Comp Physiol, 291(1): R59-R67, 2006.

STOCKER SD, Simmons JR, Stornetta RL, Toney GM, and Guyenet PG. Water deprivation activates a glutamatergic projection from the hypothalamic paraventricular nucleus to the rostral ventrolateral medulla. J Comp Neurol, 494(4): 673-685, 2006.

Other Publications