ACTH Secretion in Midbrain-Transected Rats
- 1 December 1965
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 77 (6), 1091-1096
- https://doi.org/10.1210/endo-77-6-1091
Abstract
During the first 2 days after operation "resting" plasma corticosterone levels were high, but thereafter returned to normal in both midbrain-transected and sham-operated animals. Ether anesthesia induced a significant rise in plasma corticosterone 48 hr. after midbrain transection. Three days after operation dexamethasone suppressed plasma corticosterone levels to an equivalent level in both midbrain-transected and sham-operated rats. It is concluded that the hypothalamic-adenohypophysial complex is capable of regulating ACTH release in response to selected stimulatory and inhibitory influences in midbrain-transected rats. No evidence was found to substantiate that the effect of a "tonic inhibitory neural center" on ACTH release is abolished by midbrain transection.This publication has 6 references indexed in Scilit:
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- Pathways by Which Traumatic Stress and Ether Induce Increased ACTH Release in the Rat1Endocrinology, 1964
- Studies of the Location of the Receptor Site for Negative Feedback Control of ACTH Release1Endocrinology, 1964
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- A simple fluorimetric method for the estimation of free 11-hydroxycorticoids in human plasmaJournal of Clinical Pathology, 1962
- BLOOD ACTH: EFFECTS OF ETHER, PENTOBARBITAL, EPINEPHRINE AND PAIN1Endocrinology, 1958