Morales T, Shapiro E, Mena F
Centro de Neurobiología, Universidad Nacional Autónoma de México, Campus UNAM-UAQ, 76230, Juriquilla, Qro., Mexico.
Physiol Behav. 2001;74(1-2):119-26. doi: 10.1016/s0031-9384(01)00560-1.
It is known that prolactin (PRL) is produced within the brain and numerous central actions of the hormone have been reported. In anesthetized lactating rats, central administration of PRL, i.e., intracerebroventricular (icv) or intrathecally (it), facilitated milk ejection (ME) by depressing the sympathetically mediated facilitatory tone of the mammary ductal system. However, 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 determined in both conscious and anesthetized rats. In conscious rats, the rate of ME was determined by applying a 15-min period of suckling by the litter, following a 6-h period of isolation. In anesthetized rats, intramammary pressure (IMP) responses of the mammary glands to exogenous oxytocin (OT) were recorded. The results showed that, whereas in anesthetized rats, increased responsiveness of the mammary glands to OT were observed after PRL administration, 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 mothers, this suggests that the PRL effects on ME are modulated through sympathomimetic and sympatholytic actions in conscious and anesthetized rats, respectively. Thus, as shown by ductal tone measurements, in conscious, but not in anesthetized rats, the effect of PRL was associated with increased ductal constriction within the mammary glands; an effect that was mimicked by icv administration of the beta-adrenergic agonist isoproterenol (ISOP) and 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 in conscious rats and of ISOP in anesthetized rats. Taken together, these results clearly suggest that the central effects of PRL on ME are modulated by adrenergic mechanisms.
已知催乳素（PRL）在脑内产生，并且已报道了该激素的多种中枢作用。在麻醉的泌乳大鼠中，经中枢给予PRL，即脑室内（icv）或鞘内（it）给药，可通过抑制交感神经介导的乳腺导管系统的促进性张力来促进乳汁排出（ME）。然而，尚不清楚在给PRL后，清醒大鼠是否会出现相同的效应和类似的机制。在本研究中，在清醒和麻醉大鼠中均测定了经中枢给予PRL（即icv或it）对ME的影响。在清醒大鼠中，在隔离6小时后，让一窝幼崽进行15分钟的哺乳，以此来测定ME的速率。在麻醉大鼠中，记录乳腺对外源性催产素（OT）的乳腺内压（IMP）反应。结果表明，在麻醉大鼠中，给予PRL后观察到乳腺对OT的反应性增加，而在清醒大鼠中则出现ME的强烈抑制。因为在清醒和麻醉大鼠中，事先给母鼠注射β-肾上腺素能阻滞剂普萘洛尔（PROP）可阻止这些效应，这表明PRL对ME的作用分别通过清醒和麻醉大鼠中的拟交感神经和抗交感神经作用来调节。因此，如通过导管张力测量所示，在清醒而非麻醉大鼠中，PRL的作用与乳腺内导管收缩增加有关；脑室内给予β-肾上腺素能激动剂异丙肾上腺素（ISOP）可模拟该效应，而PROP可阻止该效应。此外，脑室内给予PRL在麻醉大鼠中的抗交感神经作用可阻止脑室内给予PRL在清醒大鼠中以及ISOP在麻醉大鼠中对导管张力的影响。综上所述，这些结果清楚地表明PRL对ME的中枢作用是由肾上腺素能机制调节的。
