Journal of neuroendocrinology
-
J. Neuroendocrinol. · Feb 1993
Oxytocin pretreatment enhances arginine vasopressin-induced motor disturbances and arginine vasopressin-induced phosphoinositol hydrolysis in rat septum: a cross-sensitization phenomenon.
The recent observation that the central oxytocin (OT) receptor has high affinity for both OT and arginine vasopressin (AVP) raises the possibility that it may be involved in some of the central actions of AVP. Repeated intracerebroventricular (icv) injections of AVP in rats evoke an unusual sensitization phenomenon in that a first exposure to the peptide enhances the sensitivity (sensitization) of the brain to a second exposure. This report investigates the possibility that the OT receptor may be involved in the mediation of the phenomenon of sensitization, using OT, a specific OT receptor agonist, [Thr4,Gly7]OT, and a specific OT receptor antagonist, d(CH2)5,[Tyr(Me)2,Thr4,Tyr-NH2(9)]OVT (compound 6; cpd 6), as well as a V1 AVP receptor antagonist, d(CH2)5Tyr(Me)AVP. Peptides were injected icv in conscious, adult male Sprague-Dawley rats.(ABSTRACT TRUNCATED AT 250 WORDS)
-
J. Neuroendocrinol. · Feb 1992
Inhibition of prolactin release by gonadotropin-releasing hormone-associated Peptide in benign, dopamine-sensitive and in malignant, dopamine-resistant pituitary tumors.
Since the gonadotropin-releasing hormone-associated peptide (GAP) has been reported to be capable of inhibiting prolactin release from normal lactotrophs, with the present study we have examined the in vitro effects of GAP on prolactin release in an estrone-induced, dopamine-sensitive rat pituitary adenoma and two malignant, transplantable and dopamine-resistant rat pituitary tumors, 7315a and MtTW15. Enzymatically dispersed cells obtained from the three types of tumor were cultured in multiwell dishes for 4 days. On the fifth day, the cells were exposed for 4 h to human GAP 1-56 or to the analog GAP 42-56 or to rat GAP 1-53, at various concentrations. ⋯ Furthermore, in adenomatous cells, the inhibitory effects of these peptides were suppressed by pretreatment of the cells with pertussis toxin. These findings indicate that GAP is capable of inhibiting prolactin release even in dopamine-resistant pituitary tumors. This inhibition is exerted through a pertussis toxin-sensitive G-protein-dependent signaling mechanism in adenomatous cells.