ACTH Release Evoked by Electrical Stimulation of Brain Stem and Limbic System Sites in the Cat: The Absence of ACTH Release Upon Infundibular Area Stimulation¹

Abstract

Tissue in different parts of the brain stem and limbic system was electrically stimulated by the passage of electric current through electrodes implanted in the amygdala, hypothalamus, midbrain or medulla oblongata while plasma samples were collected for bioassay of ACTH concentration. The electrode placements were chosen so as to pass the stimulating currents through tissue in which reside neural structures implicated in control of ACTH release. Following stimulation of these structures, 3 different patterns of changes in plasma ACTH concentration occurred. Plasma ACTH levels rose promptly after stimulation at sites in the amygdaloid septal complex matching the rapidity of the response to hemorrhage or sciatic nerve stimulation. In contrast, after stimulation at sites in the medullary reticular formation, medial midbrain structures, lemniscal systems, or posterior lateral hypothalamus, the rise in plasma ACTH concentration was consistently delayed for 5–10 min, providing the basis for the suggestion that there are at least 2 different neural systems within the brain of the cat participating in ACTH release. In addition, it was found that stimulation of hypothalamic tissue at the base of the third ventricle did not elicit ACTH responses. Stimulation with current passing in either a longitudinal or a transverse direction in the neural tissue alongside the pituitary stalk in anesthetized and in awake cats failed to evoke discernible ACTH increments. This suggests that either inhibitory neurons dominate at this site or a final common path of neurons secreting CRF does not extend into the median eminence region in the cat. Another viewpoint derived from these experiments is that central nervous system mediated ACTH release is accomplished not by a single system with unified action but by separate subsystems endowed with sufficient independence to produce prompt responses and delayed responses. (Endocrinology86: 806, 1970)