Jones Juli E, Pick Rebecca R, Davenport Matthew D, Keene Alex C, Corp Eric S, Wade George N
Center for Neuroendocrine Studies, University of Massachusetts, Amherst, Massachusetts 01003, USA.
Am J Physiol Regul Integr Comp Physiol. 2002 Sep;283(3):R591-7. doi: 10.1152/ajpregu.00233.2002.
Several conditions that inhibit female sexual behavior are thought to be associated with altered corticotropin-releasing hormone (CRH) activity in the brain. The present experiments examined the hypothesis that endogenous CRH receptor signaling mediates the inhibition of estrous behavior by undernutrition and in other instances of sexual dysfunction. Intracerebroventricular (ICV) infusion of CRH or urocortin inhibited estrous behavior in ovariectomized steroid-primed hamsters. Conversely, ICV infusion of the CRH receptor antagonist astressin prevented the suppression of estrous behavior by food deprivation or by ICV administration of neuropeptide Y. Astressin treatment also induced sexual receptivity in nonresponders, animals that do not normally come into heat when treated with hormones, and this effect persisted in subsequent weekly tests in the absence of any further astressin treatment. Activation of the hypothalamo-pituitary-adrenocortical axis was neither necessary nor sufficient to inhibit estrous behavior, indicating that this phenomenon is due to other central actions of CRH receptor agonists. This is the first direct evidence that CRH receptor signaling may be a final common pathway by which undernutrition and other conditions inhibit female sexual behavior.
几种抑制雌性性行为的情况被认为与大脑中促肾上腺皮质激素释放激素（CRH）活性的改变有关。本实验检验了以下假设：内源性CRH受体信号传导介导了营养不良及其他性功能障碍情况下对发情行为的抑制。向去卵巢并用类固醇预处理的仓鼠脑室内（ICV）注射CRH或尿皮质素可抑制发情行为。相反，脑室内注射CRH受体拮抗剂阿斯特辛可防止食物剥夺或脑室内注射神经肽Y对发情行为的抑制。阿斯特辛治疗还可诱导无反应动物（即正常情况下用激素处理时不发情的动物）出现性接受能力，且在随后每周的测试中，在未进行任何进一步阿斯特辛治疗的情况下，这种效应依然存在。下丘脑-垂体-肾上腺皮质轴的激活对于抑制发情行为既非必要条件也非充分条件，这表明该现象是由CRH受体激动剂的其他中枢作用所致。这是首个直接证据，表明CRH受体信号传导可能是营养不良及其他情况抑制雌性性行为的最终共同途径。
