Hypothalamic EAP1 (enhanced at puberty 1) is required for menstrual cyclicity in nonhuman primates.

ABSTRACT: Mammalian reproductive cyclicity requires the periodic discharge of GnRH from hypothalamic neurons into the portal vessels connecting the neuroendocrine brain to the pituitary gland. GnRH secretion is, in turn, controlled by changes in neuronal and glial inputs to GnRH-producing neurons. The transcriptional control of this process is not well understood, but it appears to involve several genes. One of them, termed enhanced at puberty 1 (EAP1), has been postulated to function in the female hypothalamus as an upstream regulator of neuroendocrine reproductive function. RNA interference-mediated inhibition of EAP1 expression, targeted to the preoptic region, delays puberty and disrupts estrous cyclicity in rodents, suggesting that EAP1 is required for the normalcy of these events. Here, we sho

SUBMITTER: Dissen GA 

PROVIDER: S-EPMC3249687 | biostudies-literature | 2012 Jan

REPOSITORIES: biostudies-literature