Site of action for beta-endorphin-induced changes in plasma luteinizing hormone and prolactin in the ovariectomized rat

• Published in: Life sciences (1973) Vol. 34; no. 15; p. 1463
• Main Authors: Wiesner, J B, Koenig, J I, Krulich, L, Moss, R L
• Format: Journal Article
• Language: English
• Published: Netherlands 09.04.1984
• Subjects: Animals; beta-Endorphin; Brain - drug effects; Castration; Endorphins - pharmacology; Female; Hypothalamus, Anterior - drug effects; Hypothalamus, Middle - drug effects; Luteinizing Hormone - blood; Pituitary Gland - drug effects; Preoptic Area - drug effects; Prolactin - blood; Rats; Rats, Inbred Strains; Septum Pellucidum - drug effects
• ISSN: 0024-3205
• DOI: 10.1016/0024-3205(84)90061-4

A number of sites have been hypothesized as loci at which opioid substances act to alter the secretion of luteinizing hormone (LH) and prolactin (PRL) (1-8). The aim of the present study was to determine the site(s) at which the opioid peptide beta-endorphin (beta-END) acts to influence plasma LH and PRL levels in the ovariectomized (OVX) rat. beta-END, administered into the third ventricle of conscious OVX rats fitted with jugular catheters, significantly decreased plasma LH in doses greater than or equal to 50 ng and increased PRL levels at all doses administered (10, 50, 100 and 250 ng) in a dose dependent fashion. To identify possible central nervous system sites of action, 250 ng beta-END was unilaterally infused into various brain sites. Plasma LH was significantly decreased and plasma PRL significantly increased by infusions into the ventromedial hypothalamic area, the anterior hypothalamic area, and the preoptic-septal area. There was no significant effect of beta-END infusions into the lateral hypothalamic area, amygdala, midbrain central gray, or caudate nucleus. When hemipituitaries of OVX rats were incubated in vitro with beta-END (10(-7)M to 10(-5)M), there was no suppression of basal or LHRH-induced LH release, nor was there any alteration of basal PRL release. It is concluded that beta-END acts at a medial hypothalamic and/or preoptic-septal site and not the pituitary, to alter secretion of LH and PRL.