Kato E, Anwyl R, Quandt F N, Narahashi T
Neuroscience. 1983 Mar;8(3):643-51. doi: 10.1016/0306-4522(83)90205-1.
The response to iontophoretic application of acetylcholine in the mouse neuroblastoma cell line N1E-115 was composed of three phases. The initial fast depolarizing phase was blocked by 10 microM d-tubocurarine, but not by 0.1 microM atropine. This phase was followed by a transient hyperpolarization which in turn was followed by a secondary slow depolarization. Both the hyperpolarization and slow depolarization were blocked by atropine (0.1 microM), but not by d-tubocurarine (10 microM). The hyperpolarization and slow depolarization were also evoked by iontophoretic application of the muscarinic agonist methacholine. Under voltage-clamp conditions, an initial fast inward current, a transient outward current, and a secondary slow inward current were recorded in response to acetylcholine application. These three phases of current correspond to the three phases of the membrane potential response. The initial fast inward current increased in amplitude by hyperpolarization of the membrane, and decreased by depolarization. The mean reversal potential was estimated to be -1 mV. The outward current increased in amplitude by depolarization, decreased by hyperpolarization, and reversed its polarity at -67 mV. Alteration of external K+ concentration shifted the reversal potential in the manner expected for an increase in potassium permeability. The slow inward current increased in amplitude by hyperpolarization, decreased by depolarization, and reversed its polarity at +20 mV. It is concluded that the initial fast inward current is mediated by a nicotinic receptor similar to that in muscle end-plate membranes and in postsynaptic membranes of the sympathetic ganglia. Both the outward current and the slow inward current are mediated by muscarinic receptors. The outward current results from an increase in the membrane permeability to K+, and the slow current appears to be carried, at least in part, by Na+.
小鼠神经母细胞瘤细胞系N1E - 115对乙酰胆碱离子导入的反应由三个阶段组成。最初的快速去极化阶段可被10微摩尔的d - 筒箭毒碱阻断，但不能被0.1微摩尔的阿托品阻断。该阶段之后是短暂的超极化，接着是继发性的缓慢去极化。超极化和缓慢去极化均被阿托品（0.1微摩尔）阻断，但不被d - 筒箭毒碱（10微摩尔）阻断。毒蕈碱激动剂乙酰甲胆碱离子导入也可引发超极化和缓慢去极化。在电压钳制条件下，施加乙酰胆碱时记录到一个初始快速内向电流、一个短暂外向电流和一个继发性缓慢内向电流。这三个电流阶段与膜电位反应的三个阶段相对应。初始快速内向电流的幅度因膜超极化而增加，因膜去极化而减小。平均反转电位估计为 - 1毫伏。外向电流的幅度因膜去极化而增加，因膜超极化而减小，其极性在 - 67毫伏时反转。外部钾离子浓度的改变使反转电位按钾离子通透性增加所预期的方式发生偏移。缓慢内向电流的幅度因膜超极化而增加，因膜去极化而减小，其极性在 + 20毫伏时反转。结论是，初始快速内向电流由类似于肌肉终板膜和交感神经节突触后膜中的烟碱受体介导。外向电流和缓慢内向电流均由毒蕈碱受体介导。外向电流是由于膜对钾离子的通透性增加所致，而缓慢电流似乎至少部分由钠离子携带。
