抄録
Gonadotropin-releasing hormone (GnRH) neurons discharge action potential to release GnRH from their nerve terminals in the median eminence. It is, therefore essential, to know how the excitability of GnRH neurons is regulated. A variety of ion channels are involved in membrane excitability. Here we focus on large-conductance Ca2+ and voltage-activated K+ (BK) channels. BK channels modulate neuronal signaling by contributing to action potential repolarization, mediating the fast phase of afterhyperpolarization, and establishing a feedback loop between membrane potential and cytosolic Ca2+ that regulates release of hormones and transmitters. Overnight culture of GnRH neurons were prepared from GnRH-EGFP transgenic rats. The whole-cell currents were measured by means of the perforated patch-clamp technique at room temperature. The cell was held at -90 mV and the membrane potential was stepped to various voltages for 50 ms at 0.2 Hz. The K+ currents were activated from -30 mV and reached around 2000 pA at +60 mV. These K+ currents decreased around 30% by blocking Ca2+ channels with Ni2+ and Cd2+. The Ni2+ and Cd2+ sensitive currents were designated as the BK currents and the remained as the delayed rectifier K+ currents. In addition, BK channel blocker charybdotoxin attenuated the currents. Futhermore, RT-PCR of GnRH neurons revealed an expression of αsubunit of BK channels. Taken together, the results indicate a functional expression of BK channels in rat GnRH neurons. [J Physiol Sci. 2007;57 Suppl:S234]