Estrogen augments BK Currents in GnRH Neuronal Cell Line GT1-7.

Gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus constitute the final common path for the neuroendocrine control of reproduction. The activity of GnRH neurons is modulated by cyclic fluctuations in circulating concentration of estrogen. However, the nature of estrogen action upon these cells has not been clarified. We report here a direct action of estrogen on the regulation of potassium current, which is closely related to the neuronal excitability, in GnRH neuronal cell line, GT1-7. Delayed rectifier potassium current (I_K) and calcium-activated voltage-gated potassium (BK) current were recorded by perforated patch clamp configuration in GT1-7 cells cultured in DMEM with 10% fetal bovine serum for 3 days. BK current was increased by addition of 17β-estradiol (E2) in culture medium in a concentration-dependent manner. This action of E2 was completely blocked by ICI-182,780, a potent estrogen receptor antagonist. Acute application of E2 had no effect on the BK current. We further examined the calcium currents whether the effect by E2 on BK currents was mediated through augmentation of calcium currents. E2 had no effect on the calcium currents in GT1-7 cells. E2 exerted no effect on I_K. These results indicate that E2 increases the BK current by activating estrogen receptor without affecting calcium currents. [J Physiol Sci. 2006;56 Suppl:S217]