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  • Title: Adrenalectomy and experimental hypercorticalism modulate the basal, corticotropin-releasing-hormone- and arginine-vasopressin-stimulated release of hypothalamic beta-endorphin.
    Author: Patchev VK, Racké K, Almeida OF.
    Journal: Neuroendocrinology; 1991 Aug; 54(2):111-7. PubMed ID: 1766548.
    Abstract:
    Recent in vitro studies have shown that the release of hypothalamic beta-endorphin (beta-END), like that of adenohypophysial origin, is enhanced by both corticotropin-releasing hormone (CRH) and arginine vasopressin (AVP). However, whereas AVP merely synergizes with CRH in the pituitary, it seems to be essential for the release of hypothalamic beta-END by CRH. The present paper reports on the effects of long-term adrenalectomy (ADX) and subsequent replacement with supraphysiological doses of corticosterone (compound B, CB) upon the in vitro basal and CRH- and AVP-stimulated release of beta-END from the rat hypothalamus. Basal release of beta-END was significantly elevated by ADX, and returned to control levels following CB overdosage. Both ADX and CB replacement significantly reduced the stimulatory effect of CRH (10(-8) M) upon beta-END release. ADX caused no significant change in the AVP (10(-6) M)-induced release of beta-END. However, the AVP-stimulated release of beta-END was completely abolished in ADX rats treated with a high dose of CB. The hypothalamic content of beta-END was also measured following ADX and subsequent CB treatment. Compared with control tissues, those from ADX animals had significantly greater contents of beta-END; the hypothalami from rats with experimentally induced hypercorticalism had markedly reduced concentrations of the opioid peptide. Measurements of basal release and content of AVP in the hypothalamus following long-term ADX and CB treatment revealed that AVP neuronal activity is also subject to manipulations of the glucocorticoid hormone environment.(ABSTRACT TRUNCATED AT 250 WORDS)
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