Excitotoxic lesions of the nucleus paragigantocellularis facilitate male sexual behavior but attenuate female sexual behavior in rats.

Excitotoxic lesions of the nucleus paragigantocellularis facilitate male sexual behavior but attenuate female sexual behavior in rats.
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大鼠副巨细胞核的兴奋性毒性损伤促进雄性性行为,但减弱雌性性行为。

DOI:
10.1016/j.neuroscience.2010.11.030
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发表时间:
2011
期刊:
影响因子:
3.3
通讯作者:
Murphy,AZ
Murphy,AZ
中科院分区:
医学3区
文献类型:
--
作者:
Normandin,JJ;Murphy,AZ

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关于生殖器反射如射精和阴道收缩的下行抑制控制,我们所知甚少。脑干副巨细胞核(nPGi)投射到双侧腰骶运动神经元池,支配雄性和雌性大鼠的生殖器肌肉。电解的nPGi损伤促进男性射精,导致nPGi是下行抑制生殖器反射的来源的假设。然而,nPGi在女性性行为中的功能仍有待阐明。为此,雄性和雌性大鼠接受双侧nPGi的兴奋毒性纤维保留病变,并检查性行为和性行为诱导的Fos表达。在雄性中,nPGi损伤促进了交配,支持了nPGi而不是通道纤维是雄性大鼠生殖器反射下降抑制的来源的假设。男性nPGi病变未改变性行为诱导的任何脑区Fos表达。与基线相比,npgi损伤的雌性与受刺激的雄性交配的时间明显减少,射精返回潜伏期明显延长。这些结果与对照组女性没有显著差异,但这一趋势值得进一步分析性行为的强化价值。病变和非病变雌性对人工阴道-宫颈刺激(aVCS)形成条件位置偏好(CPP)。然而,强化后,npgi损伤的雌性在未强化室和强化室中花费的时间百分比没有差异,这表明aVCS的CPP减弱。雌性nPGi病变降低了性行为诱导的整个下丘脑和杏仁核的Fos表达。综上所述,这些结果表明,虽然雄性的nPGi病变促进了交配,但雌性的这种病变减弱了性行为的几个方面,导致交配的回报价值降低,这可能是由nPGi控制生殖器反射介导的。这项工作对理解和治疗包括延迟/早泄、不自主阴道痉挛和性交疼痛在内的性功能障碍具有重要意义。
Little is known regarding the descending inhibitory control of genital reflexes such as ejaculation and vaginal contractions. The brainstem nucleus paragigantocellularis (nPGi) projects bilaterally to the lumbosacral motoneuron pools that innervate the genital musculature of both male and female rats. Electrolytic nPGi lesions facilitate ejaculation in males, leading to the hypothesis that the nPGi is the source of descending inhibition to genital reflexes. However, the function of the nPGi in female sexual behavior remains to be elucidated. To this end, male and female rats received bilateral excitotoxic fiber-sparing lesions of the nPGi, and sexual behavior and sexual behavior-induced Fos expression were examined. In males, nPGi lesions facilitated copulation, supporting the hypothesis that the nPGi, and not fibers-of-passage, is the source of descending inhibition of genital reflexes in male rats. nPGi lesions in males did not alter sexual behavior-induced Fos expression in any brain region examined. nPGi-lesioned females spent significantly less time mating with stimulus males and had significantly longer ejaculation-return latencies compared to baseline. These results did not significantly differ from control females, but this trend warranted further analysis of the reinforcing value of sexual behavior. Both lesioned and non-lesioned females formed a conditioned place preference (CPP) for artificial vaginocervical stimulation (aVCS). However, post-reinforcement, nPGi-lesioned females did not differ in the percentage of time spent in the non-reinforced chamber versus the reinforced chamber, suggesting a weakened CPP for aVCS. nPGi lesions in females reduced sexual behavior-induced Fos expression throughout the hypothalamus and amygdala. Taken together, these results suggest that while nPGi lesions in males facilitate copulation, such lesions in females attenuate several aspects of sexual behavior resulting in a reduction in the rewarding value of copulation that may be mediated by nPGi control of genital reflexes. This work has important implications for the understanding and treatment of sexual dysfunction in people including delayed/premature ejaculation, involuntary vaginal spasms, and pain during intercourse.
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