Weiland N G, Wise P M
Department of Physiology, University of Maryland, School of Medicine, Baltimore.
Neuroendocrinology. 1989 Dec;50(6):667-72. doi: 10.1159/000125297.
Hyperprolactinemia suppresses endogenous prolactin (PRL) secretion and inhibits LH release in ovariectomized rats. Opiate peptides appear to mediate the suppressive effects of hyperprolactinemia on both endogenous PRL and LH secretion. A mechanism by which hyperprolactinemia may change the ability of opiates to influence PRL and LH is by altering the density of opiate receptors. We, therefore, examined the effect of hyperprolactinemia on the density of naloxone binding sites in hypothalamic regions that are important in the regulation of PRL and LH secretion. Female rats, ovariectomized for 4 days, were treated with ovine prolactin (oPRL) every 8 h for 2 days, and naloxone binding sites were measured using autoradiographic procedures. oPRL treatment suppressed the concentration of naloxone binding sites throughout the arcuate nucleus but had no effect in the median eminence, suprachiasmatic nucleus, and medial preoptic nucleus. There is evidence that the tuberoinfundibular dopaminergic neurons of the arcuate nucleus are directly influenced through opiate receptors. We propose that the observed decrease in the density of opiate receptors may occur on dopaminergic neurons. This theory provides an explanation for a mechanism for the suppression of endogenous PRL and LH by hyperprolactinemia: a decrease in opiate receptors will decrease opiate suppression of dopamine neurons allowing dopamine activity to increase. Increase in dopamine release are known to decrease PRL and LH secretion in ovariectomized rats. Alternatively, decreased naloxone binding may result from homologous down-regulation of receptors due to increased opiate activity. If opiate activity increases, it may directly inhibit LHRH neurons and may suppress the activity of inhibitory neurons leading to increased dopamine activity.
高催乳素血症可抑制去卵巢大鼠内源性催乳素（PRL）的分泌，并抑制促黄体生成素（LH）的释放。阿片肽似乎介导了高催乳素血症对内源性PRL和LH分泌的抑制作用。高催乳素血症可能改变阿片类物质影响PRL和LH能力的一种机制是改变阿片受体的密度。因此，我们研究了高催乳素血症对下丘脑区域纳洛酮结合位点密度的影响，这些区域在PRL和LH分泌的调节中起着重要作用。对去卵巢4天的雌性大鼠，每8小时注射一次羊催乳素（oPRL），持续2天，然后使用放射自显影程序测量纳洛酮结合位点。oPRL处理降低了整个弓状核中纳洛酮结合位点的浓度，但对正中隆起、视交叉上核和内侧视前核没有影响。有证据表明，弓状核的结节漏斗多巴胺能神经元直接受阿片受体的影响。我们认为，观察到的阿片受体密度降低可能发生在多巴胺能神经元上。这一理论为高催乳素血症抑制内源性PRL和LH的机制提供了解释：阿片受体的减少将降低阿片对多巴胺能神经元的抑制作用，从而使多巴胺活性增加。已知多巴胺释放增加会降低去卵巢大鼠的PRL和LH分泌。或者，纳洛酮结合减少可能是由于阿片活性增加导致受体同源性下调所致。如果阿片活性增加，它可能直接抑制促性腺激素释放激素（LHRH）神经元，并可能抑制抑制性神经元的活性，从而导致多巴胺活性增加。
