下丘脑去甲肾上腺素能参与纳洛酮诱导促黄体生成素释放刺激的证据。

Evidence for hypothalamic noradrenergic involvement in naloxone-induced stimulation of luteinizing hormone release.

作者信息

Van Vugt D A, Aylsworth C F, Sylvester P W, Leung F C, Meites J

出版信息

Neuroendocrinology. 1981 Nov;33(5):261-4. doi: 10.1159/000123242.

Abstract

A single injection of the opiate antagonist, naloxone (NAL), resulted in a fourfold increase in serum luteinizing hormone (LH) concentration 20 min after injection. To determine whether noradrenergic neurons were involved, male Sprague-Dawley rats were treated with alpha-methyl-p-tyrosine (alpha-MPT), phenoxybenzamine hydrochloride (PBH), or diethyldithiocarbamate (DDC), all anti-noradrenergic drugs. Reduction of hypothalamic norepinephrine synthesis by alpha-MPT or DDC, or blockade of the alpha-receptors by PBH, resulted in complete suppression of NAL-induced LH release. These results suggest that the NAL-induced increase in LH release is mediated in part via a hypothalamic noradrenergic mechanism.

摘要

单次注射阿片类拮抗剂纳洛酮（NAL）后20分钟，血清促黄体生成素（LH）浓度增加了四倍。为了确定去甲肾上腺素能神经元是否参与其中，对雄性斯普拉格-道利大鼠使用了α-甲基对酪氨酸（α-MPT）、盐酸酚苄明（PBH）或二乙基二硫代氨基甲酸盐（DDC），这些都是抗去甲肾上腺素能药物。α-MPT或DDC降低下丘脑去甲肾上腺素合成，或PBH阻断α受体，均导致NAL诱导的LH释放完全受到抑制。这些结果表明，NAL诱导的LH释放增加部分是通过下丘脑去甲肾上腺素能机制介导的。