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内源性大麻素介导急性应激和皮质酮对性行为的影响。

Endocannabinoids mediate the effects of acute stress and corticosterone on sex behavior.

作者信息

Coddington Emma, Lewis Christine, Rose James D, Moore Frank L

机构信息

Physiology and Pharmacology Department, L334, 3181 SW Sam Jackson Park Road, Oregon Health & Science University, Portland, Orgeon 97239, USA.

出版信息

Endocrinology. 2007 Feb;148(2):493-500. doi: 10.1210/en.2006-0740. Epub 2006 Nov 9.

DOI:10.1210/en.2006-0740
PMID:17095597
Abstract

For animals in the wild, survival depends on being able to detect and respond rapidly to danger by switching from risky (e.g. conspicuous courtship) to survival-oriented behaviors. Very little is known about the hormonal or neuroendocrine mechanisms that control the rapid switch in behavioral state that occurs when an animal detects threats or other stressors. Prior studies with rough-skinned newts (Taricha granulosa), an amphibian model, found that stress-induced suppression of male sexual behaviors (amplectic clasping) involves corticosterone (CORT) and that this steroid hormone uses a novel membrane receptor and modulates the responsiveness of medullary neurons in clasp-controlling neural circuits. We provide evidence that this rapid suppression of male sex behaviors, when induced by either acute stress or CORT administration, involves activation of endocannabinoids signaling in the hindbrain. In a series of behavioral studies, administration of a cannabinoid antagonist, AM281, blocked the suppressive effects of exposure to acute stress or an injection of CORT on the performance of clasping behaviors in sexually active males. Similarly, in electrophysiological studies, prior treatment with AM281 blocked CORT-induced suppression of spontaneous neuronal activity and sensory responsiveness of hindbrain neurons in clasp-controlling neural circuits. These data suggest that, in response to acute stress, elevated CORT concentration increases endocannabinoid signaling in the hindbrain and alters sexual behaviors by modulating the excitability of medullary circuits.

摘要

对于野生动物而言,生存依赖于能够通过从危险行为(如引人注目的求偶行为)转向以生存为导向的行为,来迅速察觉并应对危险。对于控制动物在察觉到威胁或其他应激源时所发生的行为状态快速转变的激素或神经内分泌机制,我们知之甚少。此前对两栖动物模式生物粗糙皮肤蝾螈(Taricha granulosa)的研究发现,应激诱导的雄性性行为(抱合行为)抑制涉及皮质酮(CORT),且这种类固醇激素使用一种新型膜受体,并调节抱合控制神经回路中髓质神经元的反应性。我们提供的证据表明,无论是急性应激还是给予CORT诱导的雄性性行为快速抑制,都涉及后脑内源性大麻素信号的激活。在一系列行为研究中,给予大麻素拮抗剂AM281可阻断急性应激暴露或注射CORT对性活跃雄性抱合行为表现的抑制作用。同样,在电生理研究中,预先用AM281处理可阻断CORT诱导的对抱合控制神经回路中后脑神经元自发神经活动和感觉反应性的抑制。这些数据表明,在急性应激反应中,升高的CORT浓度会增加后脑内源性大麻素信号,并通过调节髓质回路的兴奋性来改变性行为。

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