Töröcsik A, Vizi E S
Department of Pharmacology, Hungarian Academy of Sciences, Budapest.
J Neurosci Res. 1990 Oct;27(2):228-32. doi: 10.1002/jnr.490270213.
The effect of 4-aminopyridine, a potassium channel blocker on the muscarinic and opiate modulation of acetylcholine release, was investigated. Rat frontal cortical slices were loaded with [3H]choline, superfused continuously, and stimulated electrically. 4-Aminopyridine enhanced the stimulation-evoked release of tritium without affecting basal release. The electrically evoked release of radioactivity was reduced by the muscarinic agonist oxotremorine and the delta selective opiate receptor agonist Metenkephalin, and was enhanced in the presence of the cholinesterase inhibitor physostigmine by the muscarinic antagonist atropine. These effects were completely abolished by 4-aminopyridine. Since 4-aminopyridine blocks potassium permeability of the neuron, it is suggested that the changes in potassium permeability and the consequent alteration of membrane polarization are involved in the presynaptic modulation of acetylcholine release.
研究了钾通道阻滞剂4-氨基吡啶对毒蕈碱和阿片类物质调节乙酰胆碱释放的影响。将大鼠额叶皮质切片用[3H]胆碱加载，连续灌流，并进行电刺激。4-氨基吡啶增强了刺激诱发的氚释放，而不影响基础释放。毒蕈碱激动剂氧化震颤素和δ选择性阿片受体激动剂甲硫氨酸脑啡肽可降低放射性的电诱发释放，胆碱酯酶抑制剂毒扁豆碱存在时，毒蕈碱拮抗剂阿托品可增强放射性的电诱发释放。这些作用被4-氨基吡啶完全消除。由于4-氨基吡啶可阻断神经元的钾通透性，提示钾通透性的变化以及随之而来的膜极化改变参与了乙酰胆碱释放的突触前调节。
