Abstract
The gonadotropin-releasing hormone (GnRH) neurosecretory system constitutes the final common pathway in the neuroendocrine control of reproduction. However, the mechanisms of pulsatile and cyclic GnRH release remain poorly understood. To understand the synchronous GnRH neuron activity, which may be base of pulsatile and cyclic GnRH release, we monitored intracellular Ca2+ oscillations in GT1-7 cells and native GnRH neurons. Removal of extracellular Ca2+ abolished Ca2+ oscillations, whereas thapsigargin (inhibitor of ER Ca2+-ATPase) had no effect. Nifedipine (L-type Ca2+ channel blocker), SNX-482 (R-type blocker) and ω-conotoxin-GVIA (N-type blocker) abolished Ca2+ oscillations, indicated that Ca2+ oscillations was brought by an influx of Ca2+ through the voltage-gated Ca2+ channels. GnRH receptor (G-protein coupled receptor) antagonist abolished Ca2+ oscillations, suggested that Ca2+ oscillations were modulated by GnRH autocrine. Pertussis toxin enhanced Ca2+ oscillations, whereas H-89 (protein kinase A inhibitor) abolished Ca2+ oscillations. A high [K+]o enhanced Ca2+ oscillations in frequency and TTX (voltage-gated Na+ channel blocker) abolished Ca2+ oscillations. TEA and 4AP (voltage-gated K+ channel blocker) enhanced Ca2+ oscillations. These results suggest that Ca2+ oscillations in GnRH neurons are mediated by voltage-gated K+ channel activity affected by GnRH receptor and pertussis toxin -sensitive G protein. [J Physiol Sci. 2008;58 Suppl:S140]
