应激诱导的催乳素释放：地塞米松和纳洛酮的阻断作用可能表明存在β-内啡肽介导。
Stress-induced release of prolactin: blockade by dexamethasone and naloxone may indicate beta-endorphin mediation.
作者信息
Rossier J, French E, Rivier C, Shibasaki T, Guillemin R, Bloom F E
出版信息
Proc Natl Acad Sci U S A. 1980 Jan;77(1):666-9. doi: 10.1073/pnas.77.1.666.
Basal levels of immunoreactive (ir) beta-endorphin, corticotropin (ACTH), and prolactin (PRL) in plasma of male rats decrease after dexamethasone pretreatment (400 microgram/kg at 24 hr and 200 microgram/kg at 2 hr before). Inescapable electric footshocks increase ir-beta-endorphin, ACTH, and PRL plasma levels and this effect is blocked by dexamethasone pretreatment. Morphine (20 mg/kg) also increases ir-beta-endorphin, ACTH, and PRL levels. Dexamethasone pretreatment blocks the morphine-induced release of ir-beta-endorphin but does not prevent the morphine-induced release of PRL. Naloxone, the opiate antagonist, decreases basal plasma levels of PRL and partially blocks the stress-induced increase of PRL, but it has no effect on the basal or stress-induced release of ir-beta-endorphin. These results are consistent with the proposal that beta-endorphin may interact with an opiate receptor involved in the regulation of PRL secretion.
地塞米松预处理（在24小时前给予400微克/千克，在2小时前给予200微克/千克）后，雄性大鼠血浆中免疫反应性（ir）β-内啡肽、促肾上腺皮质激素（ACTH）和催乳素（PRL）的基础水平降低。不可逃避的电足部电击会增加ir-β-内啡肽、ACTH和PRL的血浆水平，而这种效应会被地塞米松预处理所阻断。吗啡（20毫克/千克）也会增加ir-β-内啡肽、ACTH和PRL的水平。地塞米松预处理会阻断吗啡诱导的ir-β-内啡肽释放，但不会阻止吗啡诱导的PRL释放。阿片拮抗剂纳洛酮会降低PRL的基础血浆水平，并部分阻断应激诱导的PRL增加，但对ir-β-内啡肽的基础或应激诱导释放没有影响。这些结果与β-内啡肽可能与参与PRL分泌调节的阿片受体相互作用的提议一致。
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