Kukuljan M, Stojilković S S, Rojas E, Catt K J
Laboratory of Cell Biology and Genetics, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland 20892.
FEBS Lett. 1992 Apr 13;301(1):19-22. doi: 10.1016/0014-5793(92)80201-q.
In cultured rat pituitary gonadotrophs, gonadotropin-releasing hormone (GnRH) induces rapid hyperpolarization of the cell membrane and causes cessation of the spontaneous electrical activity present in non-stimulated cells. This initial response to GnRH is followed by slow oscillations of membrane potential (Vm) which often exhibit brief bursts of action potentials (AP) fired from the peak of the oscillations. The hyperpolarization waves are synchronous with GnRH-induced elevations of cytoplasmic Ca2+ concentration ([Ca2+]i), such that Vm maxima alternate with the peak values of [Ca2+]i. The Vm oscillations result from repetitive activation of apamin-sensitive K+ channels by cytoplasmic Ca2+. Thus, GnRH activation of Ca2+ mobilization can generate a bursting pattern of membrane potential through the activation of K+ channels against a background of spontaneous electrical activity.
在培养的大鼠垂体促性腺细胞中，促性腺激素释放激素（GnRH）可诱导细胞膜迅速超极化，并使未受刺激细胞中存在的自发电活动停止。对GnRH的这种初始反应之后是膜电位（Vm）的缓慢振荡，这种振荡通常表现为从振荡峰值处激发的短暂动作电位（AP）爆发。超极化波与GnRH诱导的细胞质Ca2+浓度（[Ca2+]i）升高同步，使得Vm最大值与[Ca2+]i的峰值交替出现。Vm振荡是由细胞质Ca2+对蜂毒明肽敏感的K+通道的重复激活引起的。因此，GnRH激活Ca2+动员可在自发电活动背景下通过激活K+通道产生膜电位的爆发模式。
