FXYD1, a modulator of Na,K-ATPase activity, facilitates female sexual development by maintaining gonadotrophin-releasing hormone neuronal excitability.

ABSTRACT: The excitatory tone to gonadotrophin-releasing hormone (GnRH) neurones is a critical component underlying the pubertal increase in GnRH secretion. However, the homeostatic mechanisms modulating the response of GnRH neurones to excitatory inputs remain poorly understood. A basic mechanism of neuronal homeostasis is the Na(+),K(+)-ATPase-dependent restoration of Na(+) and K(+) transmembrane gradients after neuronal excitation. This activity is reduced in a mouse model of Rett syndrome (RTT), a neurodevelopmental disorder in which expression of FXYD1, a modulator of Na(+),K(+)-ATPase activity, is increased. We now report that the initiation, but not the completion of puberty, is advanced in girls with RTT, and that, in rodents, FXYD1 may contribute to the neuroendocrine regulation of female p

SUBMITTER: Garcia-Rudaz C 

PROVIDER: S-EPMC2934895 | biostudies-literature | 2009 Feb

REPOSITORIES: biostudies-literature