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 alpha-adrenergic antagonists, phentolamine (1 microgram/rat, i.c.v.; 29.1 +/- 4.5 ng/ml vs control 66.9 +/- 10.2 ng/ml, P less than 0.01) and tolazoline (1 microgram/rat, i.c.v.; 25.9 +/- 4.4 ng/ml vs control 59.6 +/- 10.9 ng/ml, P less than 0.05). Neither propranolol (1 microgram/rat, i.c.v.), a beta-adrenergic antagonist, nor prazosin (1 microgram/rat, i.c.v.), an alpha 1-adrenergic antagonist, inhibited pGAL-induced PRL release. Naloxone (125 micrograms/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 less than 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 less than 0.05), but the inhibition was similar to that induced by naloxone alone. These findings suggest that alpha 2-adrenergic and opioidergic mechanisms are involved in PRL release induced by GAL.