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17β-Estradiol at Physiological Concentrations Augments Ca²⁺-Activated K⁺ Currents via Estrogen Receptor β in the Gonadotropin-Releasing Hormone Neuronal Cell Line GT1-7

Department of Physiology (I.N., H.I., Y.S., M.K.), Nippon Medical School, Tokyo 113-8602, Japan; and Department of Biophysics and Biochemistry (K.U.-T., K.S.), School of Science, University of Tokyo, Tokyo 113-0033, Japan

Address all correspondence and requests for reprints to: Dr. Masakatsu Kato, Department of Physiology, Nippon Medical School, Sendagi 1, Bunkyo, Tokyo 113-8602, Japan. E-mail: mkato{at}nms.ac.jp.

Estrogens play essential roles in the neuroendocrine control of reproduction. In the present study, we focused on the effects of 17β-estradiol (E2) on the K⁺ currents that regulate neuronal cell excitability and carried out perforated patch-clamp experiments with the GnRH-secreting neuronal cell line GT1-7. We revealed that a 3-d incubation with E2 at physiological concentrations (100 pM to 1 nM) augmented Ca²⁺-activated K⁺ [K(Ca)] currents without influencing Ca²⁺-insensitive voltage-gated K⁺ currents in GT1-7 cells. Acute application of E2 (1 nM) had no effect on the either type of K⁺ current. The augmentation was completely blocked by an estrogen receptor (ER) antagonist, ICI-182,780. An ERβ-selective agonist, 2,3-bis(4-hydroxyphenyl)-propionitrile, augmented the K(Ca) currents, although an ER-selective agonist, 4,4',4''-[4-propyl-(1H)-pyrazole-1,3,5-triyl]tris-phenol, had no effect. Knockdown of ERβ by means of RNA interference blocked the effect of E2 on the K(Ca) currents. Furthermore, semiquantitative RT-PCR analysis revealed that the levels of BK channel subunit mRNAs for and β4 were significantly increased by incubating cells with 300 pM E2 for 3 d. In conclusion, E2 at physiological concentrations augments K(Ca) currents through ERβ in the GT1-7 GnRH neuronal cell line and increases the expression of the BK channel subunit mRNAs, and β4.