Abstract
Summary
The pituitary-adrenal axis of normal rats, as reflected by plasma corticoid levels, was activated acutely by the stress of ether anesthesia and withdrawal of blood by heart puncture. Bilateral electrolytic lesions in portions of the midbrain reticular formation or the amygdaloid nuclei suppressed or blocked this acute response. In such lesioned, unresponsive animals, placement of an additional lesion in hippocampus negated the block created by the first lesion in reticular formation or amygdala. The results support the opinion that hippocampus contributes an inhibitory component to the neural mechanisms regulating ACTH release.
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