Effect of dexamethasone on pituitary-adrenal activation following intrahypothalamic implantation of "neurotransmitters".

Abstract

Intrahypothalamic implantation of “neuro transmitter” substances (carbachol and norepinephrine) has previously been found to result in pituitary-adrenal activation. The present studies demonstrate that such activation is not abolished by the prior systemic administration of dexamethasone. These studies therefore support the hypothesis that the terminal hypothalamic neurosecretory neuron is steroid insensitive. (Endocrinology87: 179, 1970) THERE IS still disagreement as to whether steroid feedback regulation of adrenocortical secretion is accomplished by a direct action on the adenohypophysis (1–3), on the hypothalamus, on limbic system sites (4–6), or on all these structures. We have shown (7) that chemical implantation of minute amounts of “ neurotransmitter” substances (carbachol, an acetylcholine-like agent, and norepinephrine), when placed into the median eminence, but not in the adenohypophysis, is effective in producing an acute rise in plasma corticosteroid levels. The present studies describe the effect of prior systemic dexamethasone administration on the plasma corticosteroid (11-OHCS) responses to such intrahypothalamic implantation.