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AJP - Regulatory, Integrative and Comparative Physiology, Vol 255, Issue 5 744-R747, Copyright © 1988 by American Physiological Society
ARTICLES |
M. Irwin, R. L. Hauger, M. Brown and K. T. Britton
Clinical Center on Alcoholism, San Diego Veterans Administration Medical Center, La Jolla, California.
Corticotropin-releasing factor (CRF) acts within the brain to elicit changes in neuroendocrine, autonomic, and behavioral activity similar to those observed after stress. A reduction of immune function has also been described following central administration of CRF. In this study, we examined whether autonomic nervous system activation plays a role in CRF-induced suppression of natural killer (NK) cytotoxicity. synthetic rat CRF (1.0 microgram) microinjected into the lateral ventricle significantly increased plasma concentrations of norepinephrine and reduced splenic NK cell activity in the rat. Pretreatment of the animals with the ganglionic-blocking agent chlorisondamine completely abolished the CRF-induced increase in plasma norepinephrine levels and reduction in NK activity. However, CRF-induced elevations in plasma levels of adrenocorticotropic hormone and corticosterone were not affected by chlorisondamine. The results of this study suggest that activation of the sympathetic nervous system plays a role in CRF-induced suppression of NK cytotoxicity.
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