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High Expression of the R-Type Voltage-Gated Ca²⁺ Channel and Its Involvement in Ca²⁺-Dependent Gonadotropin-Releasing Hormone Release in GT1–7 Cells

Department of Physiology, Nippon Medical School, Tokyo 113-8602, 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: address: mkato{at}nms.ac.jp.

The GT1 cell has been widely used as a model cell to study cellular functions of GnRH neurons. Despite the importance of Ca²⁺ channels, little is known except for L- and T-type Ca²⁺ channels in GT1 cells. Therefore, we studied the diversity of voltage-gated Ca²⁺ channels in GT1–7 cells with perforated-patch clamp and RT-PCR. An R-type Ca²⁺ channel blocker, SNX-482, inhibited the Ca²⁺ currents by 75.6% in all cells examined (n = 9). A T-type Ca²⁺ channel blocker, Ni²⁺, inhibited the Ca²⁺ currents by 12.6% in all cells examined (n = 9). An L-type Ca²⁺ channel blocker, nimodipine, inhibited the Ca²⁺ currents by 17.9% in five of 11 cells examined. When using Ba²⁺ as a charge carrier, another dihydropyridine antagonist, nifedipine, clearly inhibited the currents by 12.1% in all cells examined (n = 16). An N-type Ca²⁺ channel blocker, -conotoxin-GVIA, inhibited the Ca²⁺ currents by 13.8% in three of 20 cells examined. A P/Q type Ca²⁺ channel blocker, -agatoxin-IVA, had no effect on the currents (n = 9). RT-PCR revealed that GT1–7 cells expressed the _1B, _1D, _1E, and _1H subunit mRNA. Furthermore, SNX-482 and nifedipine inhibited the high K⁺-induced increase in the intracellular Ca²⁺ concentration and GnRH release. -Conotoxin-GVIA and -agatoxin-IVA had no effect. These results suggest that GT1–7 cells express R-, L-, N-, and T-type voltage-gated Ca²⁺ channels; the R-type was a major current component, and the L-, N-, and T-types were minor ones. The R- and L-type Ca²⁺ channels play a critical role in the regulation of Ca²⁺-dependent GnRH release.

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