The study of the PGE_2 as a new sexual differentiation factor in the brain.

我们对EP受体缺失小鼠的研究表明，PGE2作为一种新的性别分化因子，与性类固醇激素的作用密切相关；睾酮治疗或睾酮剥夺均可改善EP受体缺陷小鼠的某些雄性型性行为异常。在下丘脑神经元体外分化模型中，PGE2加速了神经突伸长，这种作用是由EP4受体介导的。这些结果提示，解热镇痛药可能通过影响胎儿期神经网络的形成而诱发神经性别分化障碍。

Our study in the EP receptor-deficient mice showed that PGE2, which was suggested as a new sexual differentiation factor, was closely related to the effect of the sexual steroid hormones ; abnormalities of some male-type sexual behaviors in EP receptor-deficient mice were improved by testosterone treatment or testosterone deprivation. In the in vitro differentiation model of hypothalamic neurons, PGE2 accelerated the neurite elongation and this effect was mediated by EP4 receptor. These results indicate that antipyretic analgesic agents may have the potential to induce the disorders of neural sexual differentiation by influencing the formation of the neural network in the fetal period.