Hulse G K, Coleman G J
Pharmacol Biochem Behav. 1983 Nov;19(5):795-9. doi: 10.1016/0091-3057(83)90083-7.
The present experiments investigated the involvement of endogenous opioids in the preovulatory disruption of luteinizing hormone release and ovulation following exposure to an acute stressor. The effect of exposure to an acute stressor and/or treatment with naloxone hydrochloride on the proestrus/estrus display of lordosis behavior is also reported. Electric shocks (2 mA) delivered at 10-min intervals for three hours during the period of the preovulatory luteinizing hormone surge in adult cyclic female rats resulted in the blockage of luteinizing hormone release, decreased lordosis behavior, and inhibition of ovulation. The anti-luteinizing hormone and anti-ovulatory actions were antagonized by the administration of naloxone hydrochloride shortly prior to the application of the stressor, which suggests that the observed blockage of ovulation is mediated by endogenous opioids known to be elevated in response to a stressor. It is argued that the most likely mechanism by which endogenous opioids inhibit luteinizing hormone release and ovulation is by inhibiting luteinizing hormone releasing hormone release, and/or decreasing its production in the hypothalamus. In contrast, naloxone only partially antagonizes the anti-lordotic actions of electric shock. It is therefore further argued that the inhibition of luteinizing hormone release alone is not sufficient to explain the dramatic decrease in lordosis behavior observed following exposure to an acute stressor. Adrenal progesterone released in response to adrenocorticotropic hormone release following exposure to an acute stressor, in association with inhibited luteinizing hormone releasing hormone release is hypothesized to be responsible for the observed decrease in lordotic behavior, and the inhibition of luteinizing hormone release.
本实验研究了内源性阿片类物质在成年雌性大鼠暴露于急性应激源后促黄体生成素释放和排卵的排卵前干扰中的作用。还报道了暴露于急性应激源和/或用盐酸纳洛酮治疗对动情前期/动情期脊柱前凸行为表现的影响。在成年雌性大鼠排卵前促黄体生成素激增期间，每隔10分钟施加2毫安的电击，持续3小时，这导致促黄体生成素释放受阻、脊柱前凸行为减少以及排卵受到抑制。在施加应激源前不久给予盐酸纳洛酮可拮抗抗促黄体生成素和抗排卵作用，这表明观察到的排卵受阻是由已知因应激源而升高的内源性阿片类物质介导的。有人认为，内源性阿片类物质抑制促黄体生成素释放和排卵的最可能机制是通过抑制促黄体生成素释放激素的释放，和/或减少其在下丘脑的产生。相比之下，纳洛酮只能部分拮抗电击的抗脊柱前凸作用。因此，进一步有人认为，仅抑制促黄体生成素释放不足以解释暴露于急性应激源后观察到的脊柱前凸行为的显著减少。假设在暴露于急性应激源后，促肾上腺皮质激素释放所引发的肾上腺孕酮释放，与促黄体生成素释放激素释放受到抑制相关，是观察到的脊柱前凸行为减少和促黄体生成素释放受到抑制的原因。
