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阿片类物质和多巴胺参与精氨酸血管催产素和血管加压素诱导的雄性大鼠催乳素释放过程。

Opioid and dopamine involvement in prolactin release induced by arginine vasotocin and vasopressin in the male rat.

作者信息

Blask D E, Vaughan M K, Champney T H, Johnson L Y, Vaughan G M, Becker R A, Reiter R J

出版信息

Neuroendocrinology. 1984 Jan;38(1):56-61. doi: 10.1159/000123866.

Abstract

The potential involvement of the endogenous opioid and dopamine (DA) systems in the mechanism(s) mediating arginine vasotocin (AVT)- and arginine vasopressin (AVP)-induced prolactin (PRL) release was investigated in vivo. The injection of AVT (5 micrograms) into unanesthetized male rats resulted in a 2-fold stimulation of PRL release 15 min later, followed by an inhibition of PRL release 30 min thereafter; both the stimulatory and inhibitory PRL responses to AVT were obviated by naloxone (NAL) (200 micrograms). Similarly, the administration of either AVT or AVP (5 micrograms) to urethane-anesthetized rats led to a 3- and 5-fold increase in plasma PRL levels, respectively, 10 min after injection. The PRL stimulatory response to both peptides was completely blocked by pretreating the animals with apomorphine (APO) (5 mg); however, the injection of APO by itself had no effect on PRL secretion in these animals. Both AVT and AVP were also effective in stimulating PRL release 10 min after injection in estrogen (50 micrograms)-progesterone (25 mg) (EP)-treated rats anesthetized with urethane. APO negated the PRL stimulatory response to these compounds in the EP-treated rat as well. Normal, urethane-treated rats experienced a 7- to 8-fold increase in PRL levels 20 min following the injection of methysergide (MET) (250 micrograms). Both AVT and AVP caused approximately a 2.5-fold greater PRL response in MET-treated animals than in AVT and AVP controls, respectively; however, only in the MET + AVT-treated rats was the PRL stimulatory response greater than in the MET controls. MET probably stimulated PRL through its DA antagonistic properties.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在体内研究了内源性阿片样物质和多巴胺(DA)系统在介导精氨酸血管催产素(AVT)和精氨酸血管加压素(AVP)诱导的催乳素(PRL)释放机制中的潜在作用。向未麻醉的雄性大鼠注射AVT(5微克),15分钟后导致PRL释放增加2倍,随后30分钟后PRL释放受到抑制;纳洛酮(NAL)(200微克)消除了对AVT的PRL刺激和抑制反应。同样,向氨基甲酸乙酯麻醉的大鼠注射AVT或AVP(5微克),注射后10分钟分别导致血浆PRL水平增加3倍和5倍。用阿扑吗啡(APO)(5毫克)预处理动物可完全阻断对两种肽的PRL刺激反应;然而,单独注射APO对这些动物的PRL分泌没有影响。在氨基甲酸乙酯麻醉的经雌激素(50微克)-孕酮(25毫克)(EP)处理的大鼠中,注射后10分钟,AVT和AVP也能有效刺激PRL释放。APO也消除了EP处理大鼠中对这些化合物的PRL刺激反应。正常的、经氨基甲酸乙酯处理的大鼠在注射麦角新碱(MET)(250微克)20分钟后PRL水平增加7至8倍。与AVT和AVP对照组相比,AVT和AVP在MET处理的动物中分别引起的PRL反应大约大2.5倍;然而,只有在MET + AVT处理的大鼠中,PRL刺激反应才大于MET对照组。MET可能通过其DA拮抗特性刺激PRL。(摘要截断于250字)

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