Hyperprolactinemia decreases naloxone binding in the arcuate nucleus of ovariectomized rats.

Hyperprolactinemia decreases naloxone binding in the arcuate nucleus of ovariectomized rats.
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高催乳素血症降低了卵巢切除大鼠弓状核中纳洛酮的结合。

DOI:
10.1159/000125297
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发表时间:
1989
期刊:
影响因子:
4.1
通讯作者:
Wise,PM
Wise,PM
中科院分区:
医学2区
文献类型:
--
作者:
Weiland,NG;Wise,PM

文献摘要

被引文献

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高催乳素血症抑制去卵巢大鼠内源性催乳素(PRL)分泌并抑制LH释放。阿片肽似乎介导了高泌乳素血症对内源性PRL和LH分泌的抑制作用。高催乳素血症可能通过改变阿片受体的密度来改变阿片影响PRL和LH的能力。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,这对PRL和LH分泌的调节很重要。切除卵巢4 d的雌性大鼠,每8 h给予羊催乳素(oPRL)治疗,连续2 d,并采用放射自显像方法测量纳洛酮的结合位点。oPRL治疗抑制了整个弓形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,弓形核的结节基底多巴胺能神经元直接受到阿片受体的影响。我们认为,观察到的阿片受体密度下降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:阿片受体的减少会减少阿片对多巴胺神经元的抑制,从而使多巴胺活性增加。已知多巴胺释放的增加会减少去卵巢大鼠的PRL和LH分泌。另外,减少纳洛酮结合可能是由于阿片活性增加导致受体的同源下调。如果阿片活性增加,可能直接抑制LHRH神经元,并可能抑制抑制性神经元的活性,导致多巴胺活性增加。
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. Increases 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.