Shinozaki H, Ishida M
Brain Res. 1983 Aug 29;273(2):325-33. doi: 10.1016/0006-8993(83)90857-0.
At the crayfish neuromuscular junction chlorisondamine reduced the amplitude of both the excitatory junctional potential and the glutamate current in a dose-dependent manner in concentrations above 3 microM, and it is suggested that the drug is a powerful non-competitive antagonist for glutamate. Chlorisondamine did not act presynaptically on the crayfish neuromuscular junction. A double exponential decay of excitatory synaptic currents was observed in the presence of chlorisondamine, suggesting that this drug is an open channel blocker for the excitatory neurotransmitter. The glutamate current tail was prolonged in the presence of chlorisondamine. This prolongation increased with increasing iontophoretic current of glutamate. The rate of recovery from the refractory form of the glutamate receptor to the free reactive one was hardly affected by chlorisondamine. The inhibitory action of chlorisondamine on glutamate responses was voltage-dependent and hyperpolarization reduced the drug action. Chlorisondamine depressed the glutamate current even in Na-free, Ca-rich solution.
在小龙虾神经肌肉接头处，高于3微摩尔浓度时，氯异吲哚铵以剂量依赖方式降低兴奋性接头电位和谷氨酸电流的幅度，提示该药物是谷氨酸的强效非竞争性拮抗剂。氯异吲哚铵对小龙虾神经肌肉接头没有突触前作用。在氯异吲哚铵存在的情况下，观察到兴奋性突触电流呈双指数衰减，提示该药物是兴奋性神经递质的开放通道阻断剂。在氯异吲哚铵存在时，谷氨酸电流尾延长。这种延长随着谷氨酸离子电泳电流的增加而增加。氯异吲哚铵几乎不影响谷氨酸受体从不应期形式恢复到游离反应性形式的速率。氯异吲哚铵对谷氨酸反应的抑制作用是电压依赖性的，超极化可降低药物作用。即使在无钠、富含钙的溶液中，氯异吲哚铵也会抑制谷氨酸电流。
