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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >The inhibitory effect of anandamide on luteinizing hormone-releasing hormone secretion is reversed by estrogen.
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The inhibitory effect of anandamide on luteinizing hormone-releasing hormone secretion is reversed by estrogen.

机译：雌激素逆转了金刚烷酰胺对促黄体激素释放激素分泌的抑制作用。

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摘要

Because Delta-9-tetrahydrocannabinol (THC) inhibited luteinizing hormone-releasing hormone (LHRH) in male rats, we hypothesized that the endocannabinoid, anandamide (AEA), would act similarly. AEA microinjected intracerebroventricularly (i.c.v.) decreased plasma luteinizing hormone (LH) at 30 min in comparison to values in controls (P < 0.001). The cannabinoid receptor 1 (CB1-r)-specific antagonist, [N-(piperidin-1-yl)-1-(2,4-dichlorophenyl)-5-(4-chlorophenyl)-4-methyl-1H- pyrazole-3-carboxamide] (AM251), produced a significant elevation in plasma LH (P < 0.01). AEA (10(-9) M) decreased LHRH release from medial basal hypothalami incubated in vitro. These results support the concept that endogenous AEA inhibits LHRH followed by decreased LH release in male rats. In ovariectomized (OVX) female rats, AEA i.c.v. also inhibited LH release, but in this case AM251 had an even greater inhibitory effect than AEA. In vitro, AEA had no effect on LHRH in OVX rats. It seems that endogenous AEA inhibits LHRH followed by decreased LH release in OVX rats but that AM251 has an inhibitory action in this case. In striking contrast, in OVX, estrogen-primed (OVX-E) rats, AEA i.c.v. instead of decreasing LH, increased its release. This effect was completely blocked by previous injection of AM251. When medial basal hypothalami of OVX-E rats were incubated, AEA increased LHRH release. The synthesized AEA was higher in OVX-E rats than in OVX and males, indicating that estrogen modifies endocannabinoid levels and effects. The results are interpreted to mean that sex steroids have profound effects to modify the response to AEA. It inhibits LHRH and consequently diminishes LH release in males and OVX females, but stimulates LHRH followed by increased LH release in OVX-E-primed rats.
机译：因为Delta-9-四氢大麻酚（THC）抑制了雄性大鼠的促黄体生成素释放激素（LHRH），所以我们假设内源性大麻素，anandamide（AEA）的作用类似。与对照组相比，在30分钟时脑室内（i.c.v.）显微注射AEA可使血浆黄体生成激素（LH）降低（P <0.001）。大麻素受体1（CB1-r）特异性拮抗剂[N-（哌啶-1-基）-1-（2,4-二氯苯基）-5-（4-氯苯基）-4-甲基-1H-吡唑- 3-甲酰胺]（AM251）在血浆LH中产生显着升高（P <0.01）。 AEA（10（-9）M）降低了体外培养的内侧下丘脑内侧的LHRH释放。这些结果支持内源性AEA抑制LHRH，然后降低雄性大鼠LH释放的概念。在去卵巢（OVX）雌性大鼠中，AEA i.c.v.还可以抑制LH释放，但在这种情况下，AM251的抑制作用比AEA还要强。在体外，AEA对OVX大鼠的LHRH没有影响。内源性AEA似乎会抑制LHRH，然后在OVX大鼠中降低LH的释放，但AM251在这种情况下具有抑制作用。与之形成鲜明对比的是，在OVX中，雌激素启动（OVX-E）大鼠中，AEA i.c.v.而不是降低LH，而是增加其释放。先前注射AM251完全阻断了这种作用。当孵育OVX-E大鼠的内侧基底下丘脑时，AEA增加了LHRH的释放。 OVX-E大鼠中合成的AEA高于OVX和雄性中的AEA，表明雌激素可调节内源性大麻素的水平和作用。结果解释为，性类固醇对改变对AEA的反应具有深远的影响。它抑制LHRH，从而减少雄性和OVX雌性中的LH释放，但刺激LHRH，然后在OVX-E致敏的大鼠中增加LH释放。

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