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- Title
Correlation between the Stress-Induced Transient Increase in Corticotropin-Releasing Hormone Content of the Median Eminence of the Hypothalamus and Adrenocorticotropic Hormone Secretion.
- Authors
Murakami, Kazuharu; Akana, Susan; Dallman, Maty F.; Ganong, William F.
- Abstract
Intravenous angiotensin II and ether stress were found to produce a rapid, transient increase in the corticotropin-releasing hormone (CRH) content of the median eminence as measured by a radioimmunoassay employing an antibody against rat CRH(1-41). This confirms previous reports of transient increases in CRH measured by bioassay. The increase did not occur in the paraventricular region or in other parts of the brain. It occurred along with an increase in plasma adrenocorticotropic hormone (ACTH) when a second ether stress was administered 1 h after the first, and it also occurred when rats that had been adrenalectomized for 5 days were exposed to ether. The increases in CHR and the ACTH responses to ether were reduced or abolished by dexamethasone and pentobarbital. Four days after semicircular knife cuts in the posterior hypothalamus, resting CRH in the median eminence was increased but there was no further rise after ether stress. Plasma ACTH was normal at rest after the cuts, but the increase produced by ether was reduced. The ACTH responses to angiotensin II and immobilization were also reduced. Because the posterior knife cuts reduced hypothalamic catecholamine content, the effects of reducing hypothalamic norepinephrine and epinephrine by administration of the dopamine-β-hydroxylase inhibitor diethyldithiocarbamate (DDC) were tested. Five hours after DDC, plasma ACTH was elevated but there was no further increase with ether stress. The median eminence CRH content was normal but failed to increase after exposure to ether. The α1-adrenergic-blocking drug, prazosin, did not affect the ACTH and median eminence CRH responses to ether, but the α2-adrenergic-blocking drug, yohimbine, produced the same effects as DDC, i.e. elevated resting ACTH with no further increase following ether and a normal CRH content in the median eminence that failed to increase with ether. These results confirm the existence of a rapid, transient increase in the CRH content of the median eminence following stress and they show that stress fails to produce a similar change in other brain regions, that the increase is correleated with the occurrence of stress-induced increases in ACTH secretion, and that the increase does not occur when the ACTH response to stress is prevented. They also raise the possibility that neural pathways ascending in the brainstem are involved in the CRH and ACTH responses to ether and other stresses. Copyright © 1989 S. Karger AG, Basel
- Publication
Neuroendocrinology, 1989, Vol 49, Issue 3, p233
- ISSN
0028-3835
- Publication type
Article
- DOI
10.1159/000125122