beta-adrenergic mechanisms modulate central nervous system effects of prolactin on milk ejection

It is known that prolactin (PRL) is produced within the brain and numerous central actions of the hormone have been reported. In anesthetized lactatin g rats, central administration of PRL, i.e., intracerebroventricular (icv) or intrathecally (it), facilitated milk ejection (ME) by depressing the sym pathetically mediated facilitatory tone of the mammary ductal system. Howev er, it is not known whether or not the same effects and similar mechanisms take place in conscious rats after PRL administration. In the present study , the effects of centrally administered PRL, i.e., icv or it, on ME was det ermined in both conscious and anesthetized rats. In conscious rats, the rat e of ME was determined by applying a 15-min period of suckling by the litte r, following a 6-h period of isolation. In anesthetized rats, intramammary pressure (IMP) responses of the mammary glands to exogenous oxytocin (OT) w ere recorded, The results showed that, whereas in anesthetized rats, increa sed responsiveness of the mammary glands to OT were observed after PRL admi nistration, an intense inhibition of ME occurred in conscious rats. Because , in conscious and anesthetized rats, these effects were prevented by prior administration of the beta -adrenergic blocker propranolol (PROP) to the m others, this suggests that the PRL effects on ME are modulated through symp athomimetic and sympatholytic actions in conscious and anesthetized rats, r espectively. Thus, as shown by ductal tone measurements, in conscious, but not in anesthetized rats, the effect of PRL was associated with increased d uctal constriction within the mammary glands; an effect that was mimicked b y icv administration of the beta -adrenergic agonist isoproterenol (ISOP) a nd that was prevented by PROP. Further, the sympatholytic action of icv-PRL in anesthetized rats prevented the effect on ductal tone of both icv-PRL i n conscious rats and of ISOP in anesthetized rats. Taken together, these re sults clearly suggest that the central effects of PRL on ME are modulated b y adrenergic mechanisms. (C) 2001 Elsevier Science Inc. All rights reserved .