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Am J Physiol Regul Integr Comp Physiol 286: R123-R128, 2004; doi:10.1152/ajpregu.00328.2003
0363-6119/04 $5.00
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NEUROHUMORAL CONTROL OF CIRCULATION AND HYPERTENSION

Inactivation of the DMH selectively inhibits the ACTH and corticosterone responses to hypoglycemia

Scott B. Evans,1 Charles W. Wilkinson,1,2 Pam Gronbeck,3 Jennifer L. Bennett,1 Aryana Zavosh,1 Gerald J. Taborsky, Jr,3,4 and Dianne P. Figlewicz1,3

Departments of 1Psychiatry and Behavioral Sciences and 4Medicine, University of Washington, Seattle 98195-6560; and 3Division of Endocrinology/Metabolism and 2Geriatric Research, Education and Clinical Center, Veterans Affairs Puget Sound Health Care System, Seattle, Washington 98108

Submitted 16 July 2003 ; accepted in final form 22 September 2003

We have previously reported that repeated bouts of insulin-induced hypoglycemia (IIH) in the rat result in blunted activation of the paraventricular, arcuate, and dorsomedial hypothalamic (DMH) nuclei. Because DMH activation has been implicated in the sympathoadrenal and hypothalamic-pituitary-adrenal (HPA) responses to stressors, we hypothesized that its blunted activation may play a role in the impaired counterregulatory response that is also observed with repeated bouts of IIH. In the present study, we evaluated the role of normal DMH activation in the counterregulatory response to a single bout of IIH. Local infusion of lidocaine (n = 8) to inactivate the DMH during a 2-h bout of IIH resulted in a significant overall decrease of the ACTH response and a delay of onset of the corticosterone response compared with vehicle-infused controls (n = 9). We observed suppression of the ACTH response at time (t) = 90 and 120 min (50 ± 12 and 63 ± 6%, respectively, of control levels) and early suppression of the corticosterone response at t = 30 min (59 ± 13% of the control level). The epinephrine, norepinephrine, and glucagon responses were not altered by DMH inactivation. Our finding suggests that DMH inactivation may play a specific role in decreasing the HPA axis response after repeated bouts of IIH.

dorsomedial hypothalamus; stress; rat; lidocaine; hypothalamic-pituitary-adrenal axis


Address for reprint requests and other correspondence: D. Figlewicz Lattemann, VA Puget Sound Health Care System, Metabolism (151), 1660 South Columbian Way, Seattle, WA 98108 (E-mail: latte{at}u.washington.edu).




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