GALANIN-INDUCED PROLACTIN-RELEASE IN RATS - PHARMACOLOGICAL EVIDENCE FOR THE INVOLVEMENT OF ALPHA-ADRENERGIC AND OPIOIDERGIC MECHANISMS

The mechanism by which galanin (GAL) stimulates prolactin (PRL) secretion was investigated in urethane-anesthetized male rats. The PRL release induced by intracerebroventricular (i.c.v.) injection of porcine GAL (pGAL) was similar to that induced by rat GAL. The PRL release induced by pGAL was partially blocked by α-adrenergic antagonists, phentolamine (1 μg/rat, i.c.v.; 29.1 ± 4.5 ng/ml vs control 66.9 ± 10.2 ng/ml, P < 0.01) and tolazoline (1 μg/rat, i.c.v.; 25.9 ± 4.4 ng/ml vs control 59.6 ± 10.9 ng/ml, P < 0.05). Neither propranolol (1 μg/rat, i.c.v.), a β-adrenergic antagonist, nor prazosin (1 μg/rat, i.c.v.), an α1-adrenergic antagonist, inhibited pGAL-induced PRL release. Naloxone (125 μg/100 g body wt., i.v. 30 min before), an opiate antagonist, also inhibited pGAL-induced PRL release (25.9 ± 4.0 ng/ml vs 59.1 ± 7.2 ng/ml, P < 0.01). Combined treatment with naloxone and phentolamine caused greater inhibition of pGAL-induced PRL release than did phentolamine alone (10.3 ± 1.5 ng/ml vs 23.2 ± 4.7 ng/ml, P < 0.05), but the inhibition was similar to that induced by naloxone alone. These findings suggest that α2-adrenergic and opioidergic mechanims are involved in PRL release induced by GAL. © 1990.