Tokimasa T, Nishimura T, Akasu T
Department of Physiology, Kurume University School of Medicine, Japan.
J Auton Nerv Syst. 1988 Sep;24(1-2):123-31. doi: 10.1016/0165-1838(88)90141-5.
Intracellular recordings were made from vesical pelvic ganglion cells of the rabbit in a Krebs solution containing tetrodotoxin (1 microM). Experiments were carried out during complete suppression of the calcium-dependent potassium conductance by tetraethylammonium (greater than or equal to 20 mM) and/or intracellular injection of cesium ions. The action potential was followed by a depolarizing afterpotential which lasted for 0.3-10 s and had a peak amplitude of 5-20 mV at about -50 mV. The afterdepolarization (ADP) could not be observed when the preceding calcium-dependent action potential was blocked in a nominally calcium-free solution. Intracellular injection of ethyleneglycol-bis(beta-aminoethyl ether)N,N'-tetraacetic acid (EGTA) or total substitution of extracellular calcium ions with barium ions selectively blocked the ADP. The ADP, associated with an increased membrane conductance, reversed its polarity at -17 mV, when ganglion cells were impaled with microelectrodes filled with potassium chloride or cesium chloride. This reversal level was similar to that of the depolarization induced by gamma-aminobutyric acid. The reversal potential shifted to about -50 mV when acetate or sulphate were injected as counter anions. The peak amplitude and the total duration of the ADP was increased by substitution of external sodium chloride with sucrose or sodium isethionate. These results suggest that the ADP results from calcium entry during the spike and subsequent opening of chloride channels in parasympathetic neurons of the rabbit.
在含有河豚毒素（1微摩尔）的 Krebs 溶液中，对兔膀胱盆腔神经节细胞进行细胞内记录。实验在通过四乙铵（大于或等于20毫摩尔）完全抑制钙依赖性钾电导和/或细胞内注入铯离子的情况下进行。动作电位之后是一个去极化后电位，持续0.3 - 10秒，在约 -50毫伏时峰值幅度为5 - 20毫伏。当在名义上无钙的溶液中阻断先前的钙依赖性动作电位时，无法观察到后去极化（ADP）。细胞内注入乙二醇 - 双（β - 氨基乙醚）N，N'-四乙酸（EGTA）或用钡离子完全替代细胞外钙离子可选择性阻断ADP。当用充满氯化钾或氯化铯的微电极刺入神经节细胞时，与膜电导增加相关的ADP在 -17毫伏时反转其极性。这个反转水平与γ - 氨基丁酸诱导的去极化相似。当注入乙酸盐或硫酸盐作为抗衡阴离子时，反转电位移至约 -50毫伏。用蔗糖或羟乙基磺酸钠替代外部氯化钠会增加ADP的峰值幅度和总持续时间。这些结果表明，ADP是由于动作电位期间钙的内流以及随后兔副交感神经元中氯离子通道的开放所致。
