Department of Physiology and Institute of Basic Medical Science, Yonsei University Wonju College of Medicine, Wonju, Republic of Korea.
Neurosci Lett. 2010 Sep 27;482(2):167-71. doi: 10.1016/j.neulet.2010.07.026. Epub 2010 Jul 17.
The electrophysiological mechanism underlying afterhyperpolarization induced by the activation of the nicotinic acetylcholine receptor (nAChR) in male rat major pelvic ganglion neurons (MPG) was investigated using a gramicidin-perforated patch clamp and microscopic fluorescence measurement system. Acetylcholine (ACh) induced fast depolarization through the activation of nAChR, followed by a sustained hyperpolarization after the removal of ACh in a dose-dependent manner (10 microM to 1mM). ACh increased both intracellular Ca(2+) (Ca(2+)) and Na(+) concentrations (Na(+)) in MPG neurons. The recovery of Na(+) after the removal of ACh was markedly delayed by ouabain (100 microM), an inhibitor of Na(+)/K(+) ATPase. Pretreatment with ouabain blocked ACh-induced hyperpolarization by 67.2+/-5.4% (n=7). ACh-induced hyperpolarization was partially attenuated by either the chelation of Ca(2+) with BAPTA/AM (20 microM) or the blockade of small-conductance Ca(2+)-activated K(+) channels by apamin (500 nM). Taken together, the activation of nAChR increases Na(+) and Ca(2+), which activates Na(+)/K(+) ATPase and Ca(2+)-activated K(+) channels, respectively. Consequently, hyperpolarization occurs after the activation of nAChR in the autonomic pelvic ganglia.
使用革兰氏菌素穿孔膜片钳和显微镜荧光测量系统，研究了雄性大鼠主要盆神经节神经元（MPG）中烟碱型乙酰胆碱受体（nAChR）激活引起的超极化后电位的电生理机制。乙酰胆碱（ACh）通过激活 nAChR 引起快速去极化，随后在去除 ACh 时以剂量依赖性方式引起持续的超极化（10 microM 至 1mM）。ACh 增加 MPG 神经元中的细胞内 Ca（2+）浓度(Ca（2+）)和 Na（+）浓度(Na（+）)。哇巴因（100 microM），一种 Na（+）/K（+）ATP 酶抑制剂，可明显延迟 ACh 去除后Na（+）的恢复。哇巴因预处理使 ACh 诱导的超极化减少了 67.2+/-5.4%（n=7）。用 BAPTA/AM（20 microM）螯合Ca（2+）或用阿帕米（500 nM）阻断小电导钙激活钾通道，均可部分减弱 ACh 诱导的超极化。综上所述，nAChR 的激活增加了Na（+）和Ca（2+），分别激活了 Na（+）/K（+）ATP 酶和钙激活钾通道。因此，nAChR 在自主盆神经节中的激活后会发生超极化。
