Lack of involvement of dopamine and serotonin during the orphanin FQ/Nociceptin (OFQ/N)-induced prolactin secretory response.
Lack of involvement of dopamine and serotonin during the orphanin FQ/Nociceptin (OFQ/N)-induced prolactin secretory response.
复制标题
在孤啡肽 FQ/痛敏肽 (OFQ/N) 诱导的催乳素分泌反应过程中缺乏多巴胺和血清素的参与。
DOI：
10.1016/j.lfs.2005.04.010
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发表时间：
2005
期刊：
影响因子：
6.1
通讯作者：
Janik,James
中科院分区：
文献类型：
--
作者：
Kraska,Amy;Bryant,Winnifred;Murphree,Emily;Callahan,Phyllis;Janik,James
这些研究的目的是研究孤啡肽/孤啡肽（OFQ/N）诱导催乳素释放的可能机制。我们研究了多巴胺能神经元的参与，通过定量DOPAC：DA水平的正中隆起和神经中间叶后，中央管理OFQ/N雌性SD大鼠。为了明确结节漏斗多巴胺能神经元的参与，进行免疫细胞化学研究，以观察孤啡肽/N中枢给药后弓状核中c-fos蛋白的表达。此外，使用选择性5-羟色胺拮抗剂ritansarin和非选择性拮抗剂metergoline进行剂量反应研究，检查了多巴胺能激活的作用。最后，催乳素反应的药理学特异性通过用[Nphe 1] NC（1-13）NH 2（一种据报道可拮抗OFQ/N效应的药物）预处理动物来检查。这些研究的结果表明，增加催乳素释放后，中央管理OFQ/N不抑制tuberoinfundibular，tuberohypophyseal或脑室周围垂体多巴胺能神经元的活动，在10分钟后，药物给药，催乳素水平显着升高的时间。此外，由于对多巴胺能受体的药理学阻断并不改变对OFQ/N的催乳素分泌反应，因此不涉及多巴胺能激活。NC（1-13）NH_2不拮抗OFQ/N对催乳素分泌的刺激作用。OFQ/N对多巴胺能神经元活性的神经效应可能发生在与催乳素增加不同的时间过程之后。
The purpose of these studies was to examine possible mechanisms of Orphanin FQ/Nociceptin (OFQ/N)-induced prolactin release. We investigated the involvement of the dopaminergic neurons by quantifying DOPAC:DA levels in the median eminence and neurointermediate lobe following central administration of OFQ/N to female Sprague–Dawley rats. To specifically determine the involvement of the tuberoinfundibular dopaminergic neurons, immunocytochemical studies were conducted to visualize c-fos protein expression in the arcuate nucleus following central administration of OFQ/N. In addition, the role of serotonergic activation was examined in dose response studies using the selective serotonin antagonist ritansarin and the nonselective antagonist metergoline. Finally, the pharmacological specificity of the prolactin response was examined by pretreating animals with [Nphe1] NC (1–13)NH2, a drug reported to antagonize OFQ/N effects. The results of these studies indicate that the increase in prolactin release following central administration of OFQ/N does not inhibit tuberoinfundibular, tuberohypophyseal or periventricular hypophysial dopaminergic neuronal activity at 10 min after drug administration, a time when prolactin levels were significantly elevated. Furthermore, serotonergic activation is not involved since pharmacological blockade of serotonergic receptors did not alter the prolactin secretory response to OFQ/N. NC (1–13)NH2did not antagonize the stimulatory effects of OFQ/N on prolactin secretion. The neural effects of OFQ/N on dopaminergic neuronal activity may occur following a different time course than that of the prolactin increase.