Enhanced At Puberty 1 (EAP1)

Eap1, increased in the medial basal hypothalamus, but not cerebral cortex, of female rhesus monkeys at early puberty and increased further at midpuberty. Female mice underwent a similar increase of Eap1 expression in hypothalamus, but not cortex, during puberty. In situ hybridization showed that Eap1 mRNA was abundant in cells of hypothalamic nuclei involved in Gnrh secretion, such as the arcuate nucleus. Immunohistochemical analysis localized Eap1 to cell nuclei. Inhibition of Eap1 by RNAi targeted to the preoptic area of female rats disrupted the estrous cycle and reduced plasma gonadotropin levels, suggesting altered Gnrh release. These abnormalities were accompanied by stunted antral follicular development and formation of ovarian cysts.