Responsiveness of Adenohypophysial Corticotrophs to Hypothalamic (SME) Extract Remains Unchanged in Rats with Hypothalamic Lesions Inhibiting CRF Release

Abstract

The corticotrophin-releasing activity of stalk-median eminence (SME) extract was studied using incubated quarters of anterior pituitary glands obtained from rats with long-term anterolateral deafferentation or complete surgical lesion of the medial basal hypothalamus, as well as with the lesion of the paraventricular nuclei. These hypothalamic interventions are known to cause a complete or partial but significant deficiency in hypothalamic corticotrophin-releasing factor (CRF) release, however, such lesions failed to alter the sensitivity of the ACTH response from incubated pituitary segments towards the SME extract. These results suggest that the specific responsiveness of adenohypophysial corticotrophs is maintained when hypothalamic CRF supply is decreased for a long period of time.

Hypothalamic Control of Adrenocorticotropin Secretion: Advances since the Discovery of 41-Residue Corticotropin-Releasing Factor

“…Various modes of destroying the hypothalamo-hypophysial CRF pathway failed to cause any marked alteration in the sensitivity (ED 50 ) or the capacity (V max ) of pituitary segments to release ACTH in response to CRF-41 (209), vasopressin (241), or hypothalamic extracts (242) in vitro. Moreover, there is no sign of an upregulation of either CRF-41 (Holmes, M. C, and F. A. Antoni, unpublished data) or vasopressin receptors (226,229) after hypothalamic lesions that destroy CRF neurons.…”

“…This finding may be explained by the weakened glucocorticoid feedback in these animals. In humans the main determinant of the pituitary response to CRF-41 appears to be the glucocorticoid status of the subjects (74), and work in rats also points in this direction (224,(236)(237)(238)(239)(240)(241)(242)(243).…”