Pfaus J G, Jakob A, Kleopoulos S P, Gibbs R B, Pfaff D W
Department of Psychology, Concordia University, Montréal, Canada.
Neuroendocrinology. 1994 Sep;60(3):283-90. doi: 10.1159/000126760.
We have shown previously that sexual stimulation (copulation with intromission or vaginocervical stimulation) induces c-fos mRNA and Fos-like immunoreactivity (IR) within estrogen-concentrating and nonconcentrating regions of the female rat forebrain, including regions that contain gonadotropin-releasing hormone (GnRH) neurons in septum and anterior preoptic area. The overall induction of Fos-like IR within these regions was specific to afferent sensory stimulation and did not require treatment with estrogen and progesterone. Because vaginocervical stimulation facilitates lordosis and increases the release of luteinizing hormone, the present study examined whether hormone treatment that promotes sexual receptivity, with or without sexual stimulation, increases Fos-like IR specifically within GnRH-containing neurons. Sexually experienced ovariectomized rats were administered estradiol benzoate (10 micrograms) 48 h and progesterone (500 micrograms) 4 h before either 1 h of paced copulation with a sexually vigorous male, 50 vaginocervical stimulations with a glass rod distributed over 1 h, or no stimulation. Control rats received injections of the oil vehicle. Fos-like IR was found within a significant number of GnRH-positive neurons in the anterior preoptic area caudal to the organum vasculosum following copulation with intromission or vaginocervical stimulation as compared with no stimulation. Although few GnRH cells coexpressed Fos following hormone treatment alone, this treatment enhanced the number of GnRH neurons that coexpressed Fos following vaginocervical stimulation as compared with the effect of vaginocervical stimulation in oil-treated rats. Together, these data indicate that estrogen and progesterone can augment the responsiveness of certain GnRH neurons to vaginocervical stimulation, consistent with the effects of sexual activity on GnRH release.
我们之前已经表明,性刺激(插入式交配或阴道-宫颈刺激)可诱导雌性大鼠前脑雌激素浓集和非浓集区域内的c-fos mRNA和Fos样免疫反应性(IR),包括在隔区和视前区前部含有促性腺激素释放激素(GnRH)神经元的区域。这些区域内Fos样IR的总体诱导对传入感觉刺激具有特异性,并且不需要雌激素和孕酮处理。由于阴道-宫颈刺激促进脊柱前凸并增加促黄体生成素的释放,本研究检测了促进性接受性的激素处理(无论有无性刺激)是否会特异性增加含GnRH神经元内的Fos样IR。对有性经验的去卵巢大鼠,在与性活跃雄性进行1小时有节奏的交配、用玻璃棒在1小时内进行50次阴道-宫颈刺激或不进行刺激之前48小时给予苯甲酸雌二醇(10微克),4小时前给予孕酮(500微克)。对照大鼠注射油剂。与无刺激相比,在插入式交配或阴道-宫颈刺激后,视前区前部尾侧至血管器的大量GnRH阳性神经元内发现了Fos样IR。虽然单独激素处理后很少有GnRH细胞共表达Fos,但与油剂处理大鼠中阴道-宫颈刺激的效果相比,这种处理增强了阴道-宫颈刺激后共表达Fos的GnRH神经元的数量。总之,这些数据表明雌激素和孕酮可以增强某些GnRH神经元对阴道-宫颈刺激的反应性,这与性活动对GnRH释放的影响一致。