Croxton T L, Ben-Jonathan N, Armstrong W M
Department of Physiology and Biophysics, Indiana University School of Medicine, Indianapolis 46223.
Endocrinology. 1988 Oct;123(4):1783-91. doi: 10.1210/endo-123-4-1783.
Electrophysiological studies were performed to characterize membrane currents of rat gonadotropes under basal conditions and after exposure to secretagogues. Gonadotropes were identified in primary cultures of rat anterior pituitaries by a reverse hemolytic plaque assay. Giga-seal patch clamp recording with the cell-attached configuration was used to monitor membrane currents in these cells. Spontaneous spikes in basal current were seen. These were blocked by methoxyverapamil and probably reflect Ca2+-dependent action potentials. Brief GnRH stimulation induced slow oscillatory changes in membrane current that evolved into a series of large amplitude inward pulses after about 8 min. Treatment with TRH had no effect, and depolarization with K+ led to delayed inward currents without any oscillatory behavior. Under conditions of Ca2+ channel blockade, GnRH stimulation did not induce pulses of inward current, but did lead to oscillatory activation of a small conductance ion channel apparently selective for K+. Taken together these results suggest that GnRH induces oscillations in intracellular Ca2+ and that these oscillations are controlled by biochemical processes.
进行电生理研究以表征大鼠促性腺激素细胞在基础条件下以及暴露于促分泌素后的膜电流。通过反向溶血空斑试验在大鼠垂体前叶的原代培养物中鉴定促性腺激素细胞。采用细胞贴附式配置的千兆封接膜片钳记录来监测这些细胞中的膜电流。在基础电流中可见自发尖峰。这些尖峰被甲氧基维拉帕米阻断,可能反映了钙依赖性动作电位。短暂的促性腺激素释放激素(GnRH)刺激诱导膜电流发生缓慢的振荡变化,约8分钟后演变为一系列大幅度内向脉冲。促甲状腺激素释放激素(TRH)处理没有效果,钾离子去极化导致延迟的内向电流,没有任何振荡行为。在钙通道阻断的条件下,GnRH刺激不会诱导内向电流脉冲,但会导致一个明显对钾离子有选择性的小电导离子通道的振荡激活。综合这些结果表明,GnRH诱导细胞内钙离子振荡,并且这些振荡受生化过程控制。