Georgescu Michaela, Sabongui Camille, Del Corpo Adina, Marsan Lina, Pfaus James G
Center for Studies in Behavioral Neurobiology, Department of Psychology, Concordia University, Montréal, QC, Canada.
Horm Behav. 2009 Oct;56(4):450-6. doi: 10.1016/j.yhbeh.2009.07.014. Epub 2009 Aug 7.
Vaginocervical stimulation (VCS) induces the immediate-early gene product Fos in the ventromedial hypothalamus (VMH) of female rats. However, this induction is lower in ovariectomized rats that receive estradiol benzoate (EB) and progesterone (P) relative to an oil vehicle. We have observed that a substantial proportion of cells activated in the VMH by VCS stain for glutamate, and infusions of glutamate or its selective receptor agonists to the VMH inhibit both appetitive and consummatory sexual behaviors in females. This raises the possibility that VCS activates an inhibitory glutamate system in the VMH, and that ovarian steroids blunt the activation, although it is not known whether EB or P, alone or in combination, lead to this effect. The present experiment examined the ability of VCS to induce Fos in glutamate neurons in the VMH of ovariectomized rats under 4 hormonal regimens: oil, EB alone, P alone, or EB+P, following 1 or 50 distributed VCSs administered with a lubricated glass rod over the course of 1 h. Treatment with EB or P alone significantly reduced the number of glutamate neurons activated by 1 VCS, with P being more effective than EB. Treatment with EB+P also produced a significant reduction, but not to the extent of EB or P alone. Although EB and P work in synergy to activate sexual behavior in female rats, actions of EB or P alone are sufficient to blunt the ability of VCS to activate glutamate neurons in the VMH. It thus appears that ovarian steroids may "disinhibit" sexual responding, in part, by dampening the ability of VCS to activate glutamate neurons in the VMH. In turn, this may allow females to receive a sufficient number of intromissions for the activation of sexual reward and the facilitation of pregnancy.
阴道宫颈刺激（VCS）可诱导雌性大鼠腹内侧下丘脑（VMH）中即早基因产物Fos的表达。然而，相对于接受油剂的去卵巢大鼠，接受苯甲酸雌二醇（EB）和孕酮（P）的去卵巢大鼠中这种诱导作用较低。我们观察到，VCS在VMH中激活的细胞中有很大一部分对谷氨酸染色，并且向VMH中注入谷氨酸或其选择性受体激动剂会抑制雌性的求偶和性行为。这就提出了一种可能性，即VCS激活了VMH中的抑制性谷氨酸系统，而卵巢类固醇会减弱这种激活，尽管尚不清楚是EB还是P单独或联合导致了这种效应。本实验研究了在4种激素方案下，VCS诱导去卵巢大鼠VMH中谷氨酸能神经元Fos表达的能力：油剂、单独使用EB、单独使用P或EB + P，在1小时内用润滑玻璃棒进行1次或50次分散的VCS刺激。单独使用EB或P处理显著减少了由1次VCS激活的谷氨酸能神经元数量，P比EB更有效。EB + P处理也产生了显著减少，但程度不如单独使用EB或P。尽管EB和P协同作用激活雌性大鼠的性行为，但单独使用EB或P的作用足以减弱VCS激活VMH中谷氨酸能神经元的能力。因此，卵巢类固醇似乎可能部分通过减弱VCS激活VMH中谷氨酸能神经元的能力来“解除抑制”性反应。反过来，这可能使雌性能够接受足够数量的插入以激活性奖励并促进怀孕。
