Galanin stimulates luteinizing hormone-releasing hormone secretion from arcuate nucleus-median eminence fragments in vitro: involvement of an alpha-adrenergic mechanism.

Galanin (GAL), a 29-amino acid peptide originally isolated from porcine intestine, has been shown to be widely distributed not only in the gut, but also in the central nervous system. Several studies have shown that GAL participates in the hypothalamic regulation of PRL, GH, and LH secretion. In this study, we evaluate the effects of rat GAL (rGAL) on LHRH and prostaglandin (PG) E2 release from arcuate nucleus-median eminence fragments in vitro. Fragments were incubated for 30-min periods in Krebs-Ringer bicarbonate buffer containing the different test substances. The addition to the medium of rGAL in concentrations ranging from 5-1000 nM increased the release of both LHRH and PGE2 in a concentration-dependent manner. The ED50 values were approximately 55 and 80 nM for LHRH and PGE2, respectively. rGAL-induced LHRH and PGE2 release were related, as suggested by the finding that the addition to the medium of indomethacin (10 microM), a PG synthesis blocker, completely blocked rGAL-induced LHRH release. In addition, an active catecholaminergic system appears to be necessary for obtaining the stimulatory effect of rGAL. The addition to the medium of the alpha-adrenergic blocker phentolamine or prazosin impaired the ability of rGAL to release both LHRH and PGE2. rGAL-induced stimulation of LHRH and PGE2 release was blocked by phentolamine at doses of 1-10 microM, while prazosin was able to block it at doses as low as 0.1 microM. In summary, rGAL stimulates LHRH and PGE2 release from arcuate nucleus-median eminence fragments in vitro in a dose-dependent fashion. Such an effect is blocked by both indomethacin and alpha-adrenergic blockers, indicating that rGAL-induced stimulation of LHRH secretion is exerted through alpha-adrenergic receptors and requires PGE2 as an intracellular mediator.