Supression of basal and stress-induced prolactin release and stimulation of luteinizing hormone secretion by α-melanocyte-stimulating hormone

Abstract

α-MSH and β-endorphin, both synthesized from a common precursor, have opposite behavioral actions. In order to determine if these peptides have opposite effects on pituitary function, basal LH secretion and basal and stress-induced prolactin release were studied in adult male rats after intraventricular injection of α-MSH. Each rat also received intraventricular saline in order to serve as its own control. 18 μg α-MSH stimulated plasma LH from 16.5 ± 2.5 (SEM) ng/ml to a peak of 27.2 ± 4.0 and 26.0 ± 4.9 n g/ml at 5 and 10 min, and suppressed prolactin from 3.5 ± 0.7 ng/ml to 1.3 ± 0.1 and 1.2 ± 0.1 ng/ml at 15 and 30 min. Intraventricular α-MSH also significantly blunted the prolactin rise associated with the stress of swimming. 10 and 20 min after the onset of swimming, prolactin levels in rats pretreated with α-MSH were significantly diminished: 7.4 ± 1.5 and 6.5 ± 2.0 ng/ml vs 23.8 ± 3.6 and 15.2 ± 2.8 after normal saline. Similarly, des-acetyl α-MSH which is the predominant form of α-MSH in the hypothalamus, diminished the stress-induced prolactin rise from 18.4 ± 5.3 and 11.2 ± 3.4 ng/ml at 10 and 20 min to 10.0 ± 2.4 and 5.5 ± 1.6 ng/ml. We conclude that centrally administered α-MSH stimulates LH and suppresses basal and stress-induced prolactin release in male rats. These actions are opposite to those previously shown for β-endorphin and suggest that α-MSH may antagonize the effects of β-endorphin on pituitary function.