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Submitted on September 19, 2003
Accepted on January 13, 2004
Department of Physiology, Nippon Medical School, Tokyo 113-8602, Japan
* To whom correspondence should be addressed. E-mail: 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 5 out of 11 cells examined. When using Ba2+ as a charge carrier, another dihydropiridine 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 3 out 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 and the R-type was a major current component, and the L- N- and T-type 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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