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AJP - Regulatory, Integrative and Comparative Physiology, Vol 259, Issue 4 799-R806, Copyright © 1990 by American Physiological Society
ARTICLES |
M. Egawa, H. Yoshimatsu and G. A. Bray
Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033.
To investigate the sites of action of corticotropin-releasing hormone (CRH) on sympathetic nerve activity to interscapular brown adipose tissue (IBAT), we injected CRH into the third cerebroventricle, medial preoptic area (MPOA), and other hypothalamic areas in anesthetized rats. The multiunit discharges of sympathetic nerves to IBAT were recorded electrophysiologically. The intracerebroventricular injection of CRH increased sympathetic nerve activity in a dose-dependent manner over the range 250-1,000 pmol. The microinjection of CRH (200 pmol) into the unilateral MPOA increased the sympathetic nerve activity to IBAT by +150.6 +/- 25.9% at 30 min after injection. However, the injection of saline (0.15 M NaCl) and glucagon (200 pmol) into the MPOA did not increase sympathetic nerve activity. The microinjection of CRH (200 pmol) into the anterior hypothalamic area, paraventricular hypothalamic nucleus, ventromedial hypothalamic nucleus, and lateral hypothalamic area had no significant effect on nerve activity. We conclude that central administration of CRH increases the sympathetic nerve activity to IBAT and that the MPOA is one of the sites for this action. The result is consistent with the hypothesis that CRH is a neurochemical stimulator of the sympathetic nervous system, which may be involved in control of energy expenditure in rodents.
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