Lees G M, Wallis D I
Br J Pharmacol. 1974 Jan;50(1):79-93. doi: 10.1111/j.1476-5381.1974.tb09595.x.
1 The mechanisms underlying the hyperpolarization which follows depolarization of rabbit superior cervical ganglion cells by acetylcholine, have been investigated and compared with the mechanisms responsible for the hyperpolarizations induced by orthodromic stimulation of the ganglion.2 The amplitude of the drug-induced hyperpolarization (after-hyperpolarization) was diminished when Na(+) and the duration of the preceding depolarization were reduced.3 In K(+)-free solutions, the amplitude of the after-hyperpolarization was often diminished and its rate of development was reduced. In 12.5 mM K(+)-Krebs solutions, the amplitude and rate of development of the after-hyperpolarization were increased; the potential was still present when the resting potential was at or close to E(K).4 Ouabain (10 muM) prevented or greatly diminished the after-hyperpolarization. The rates of onset and decay of the after-hyperpolarization were reduced in glucose-free solutions.5 It is, therefore, concluded that the after-hypolarization is due to the activity of an electrogenic sodium pump.6 The positive after-potential associated with the ganglionic action potential was increased in K(+)-free solutions and diminished when the resting potential approached E(K), indicating that it is due to a period of increased K(+) conductance. In the presence of high concentrations of hexamethonium (276 muM), the P wave was not selectively depressed by ouabain and has been shown by other workers to be due to a mechanism not involving an increased potassium conductance. It is concluded, therefore, that the positive after-potential, the P wave and the after-hyperpolarization are due to different mechanisms.
对乙酰胆碱使兔颈上神经节细胞去极化后随之发生的超极化的机制进行了研究，并与神经节顺向刺激所诱导的超极化的机制进行了比较。
当[Na⁺]₀和先前去极化的持续时间减小时，药物诱导的超极化（后超极化）幅度减小。
在无钾溶液中，后超极化的幅度常常减小，其发展速率降低。在12.5 mM钾的 Krebs 溶液中，后超极化的幅度和发展速率增加；当静息电位处于或接近 E(K)时，该电位仍然存在。
哇巴因（10 μM）可阻止或大大减小后超极化。在无葡萄糖溶液中，后超极化的起始和衰减速率降低。
因此，得出结论：后超极化是由于生电钠泵的活动所致。
与神经节动作电位相关的正后电位在无钾溶液中增加，而当静息电位接近 E(K)时减小，表明它是由于钾电导增加的一段时间所致。在高浓度六甲铵（276 μM）存在时，P 波不会被哇巴因选择性抑制，其他研究者已表明它是由一种不涉及钾电导增加的机制引起的。因此，得出结论：正后电位、P 波和后超极化是由不同机制引起的。
