Lamarca M V, Collier B
J Pharmacol Exp Ther. 1983 Jul;226(1):249-57.
These experiments tested the effect of 4-aminopyridine (4-AP) on acetylcholine (ACh) release, 45Ca++ accumulation and transmission in the perfused superior cervical ganglion of the cat. The 4-AP increased the amount of ACh released during preganglionic nerve stimulation, but it did not alter spontaneous ACh release. The 4-AP-induced increase of ACh release was compensated for by increased ACh synthesis because stimulation in the presence of the drug did not deplete tissue ACh content. When ACh release was suppressed by Mg++ or by low Ca++, 4-AP restored release to normal, but it did not do so when Ca++ was absent. This is interpreted as consistent with the idea that 4-AP increases Ca++ influx into nerve terminals and this was supported by measures of 45Ca++ accumulation by ganglia. Thus, preganglionic nerve stimulation increased 45Ca++ accumulation by ganglia and 4-AP increased this measure; Mg++ decreased the stimulation-induced change in 45Ca++ accumulation and 4-AP reversed this effect of Mg++. Depression of ganglionic transmission caused by Mg++ was readily antagonized by 4-AP, but the compound did not as readily augment transmission depressed by tubocurarine or by trimethaphan.
这些实验测试了4-氨基吡啶（4-AP）对猫的灌注颈上神经节中乙酰胆碱（ACh）释放、45Ca++积累及传递的影响。4-AP增加了节前神经刺激期间释放的ACh量，但未改变ACh的自发释放。4-AP诱导的ACh释放增加通过ACh合成增加得到补偿，因为在药物存在下刺激并未耗尽组织中的ACh含量。当ACh释放被Mg++或低Ca++抑制时，4-AP可将释放恢复正常，但在无Ca++时则不能。这被解释为与4-AP增加Ca++流入神经末梢的观点一致，神经节对45Ca++的积累测量结果支持了这一点。因此，节前神经刺激增加了神经节对45Ca++的积累，4-AP增强了这一效应；Mg++降低了刺激诱导的45Ca++积累变化，而4-AP逆转了Mg++的这一效应。Mg++引起的神经节传递抑制很容易被4-AP拮抗，但该化合物对筒箭毒碱或三甲噻方引起的传递抑制增强作用不明显。
