Valdez Susana R, Pennacchio Gisela E, Gamboa Dante F, de Di Nasso Elina G, Bregonzio Claudia, Soaje Marta
Laboratorio de Reproducción y Lactancia, IMBECU-CONICET, Mendoza, Argentina; Instituto de Ciencias Básicas, Universidad Nacional de Cuyo, Mendoza, Argentina.
Laboratorio de Reproducción y Lactancia, IMBECU-CONICET, Mendoza, Argentina.
Pharmacol Rep. 2014 Jun;66(3):386-93. doi: 10.1016/j.pharep.2013.12.006. Epub 2014 Apr 3.
The opioid system modulates prolactin release during late pregnancy. Its role and the participation of ovarian hormones in this modulation are explored in ether stress-induced prolactin release.
METHODS/RESULTS: Estrous, 3-day and 19-day pregnant rats were used. We administered the antagonist mifepristone (Mp) and tamoxifen to evaluate progesterone and estradiol action in naloxone (NAL, opioid antagonist) or saline treated rats. Ether stress had no effect on serum prolactin levels in controls but increased prolactin release in NAL-treated rats. Prolactin response to stress in NAL-treated rats was blocked by l-DOPA administration. Mp treatment on day 18 of pregnancy increased prolactin levels after stress without alterations by NAL. Tamoxifen on days 14 and 15 of pregnancy completely blocked Mp and NAL effects on prolactin release at late pregnancy. In contrast, stress significantly increased prolactin levels in estrous rats and pretreatment with NAL prevented this. On day 3 of pregnancy, at 6.00 p.m., stress and NAL treatment inhibited prolactin levels in saline-treated rat. No effect of stress or NAL administration was detected on day 3 of pregnancy at 9.00 a.m. icv administration of specific opioids antagonist, B-Funaltrexamine but not Nor-Binaltorphimine or Naltrindole, caused a significant increase in stress-induced prolactin release.
Opioid system suppression of prolactin stress response during late pregnancy was observed only after progesterone withdrawal, involving a different opioid mechanism from its well-established stimulatory role. This mechanism acts through a mu opioid receptor and requires estrogen participation. The opioid system and progesterone may modulate stress-induced prolactin release, probably involving a putative prolactin-releasing factor.
阿片系统在妊娠晚期调节催乳素释放。本研究在乙醚应激诱导的催乳素释放中探讨其作用以及卵巢激素在这种调节中的参与情况。
方法/结果：使用动情期、妊娠3天和19天的大鼠。我们给予拮抗剂米非司酮（Mp）和他莫昔芬，以评估孕酮和雌二醇在纳洛酮（NAL，阿片拮抗剂）或生理盐水处理的大鼠中的作用。乙醚应激对对照组血清催乳素水平无影响，但增加了NAL处理大鼠的催乳素释放。给予左旋多巴可阻断NAL处理大鼠对应激的催乳素反应。妊娠第18天给予Mp可增加应激后催乳素水平，且不受NAL影响。妊娠第14天和15天给予他莫昔芬可完全阻断Mp和NAL对妊娠晚期催乳素释放的影响。相比之下，应激显著增加了动情期大鼠的催乳素水平，而预先给予NAL可预防这种情况。在妊娠第3天下午6点，应激和NAL处理抑制了生理盐水处理大鼠的催乳素水平。在妊娠第3天上午9点，未检测到应激或给予NAL的影响。脑室内给予特异性阿片拮抗剂β-氟纳曲明，但不是去甲二氢吗啡酮或纳曲吲哚，可导致应激诱导的催乳素释放显著增加。
仅在孕酮撤退后观察到阿片系统在妊娠晚期对催乳素应激反应的抑制作用，涉及一种与其已确立的刺激作用不同的阿片机制。该机制通过μ阿片受体起作用，且需要雌激素参与。阿片系统和孕酮可能调节应激诱导的催乳素释放，可能涉及一种假定的催乳素释放因子。
