Drozdova E I, Pivovarov A S, Robakidze T N
All-Union Scientific Center for the Safety of Biologically Active Substances, Staraya Kupavna. M.V. Lomonosov Moscow State University.
Neurosci Behav Physiol. 1994 Nov-Dec;24(6):507-12. doi: 10.1007/BF02360176.
The influence of amiridin and tacrine on the membrane potential, activity, and plasticity of cholinoreceptors was investigated using the methods of recording of intracellular potentials and transmembrane currents in identified RPa3 and LPa3 neurons of the common snail. Amiridin and tacrine (1-100 mumole/liter) do not exert appreciable influences on the membrane potential of the cells. Both compounds modulate the activity of cholinoreceptors, judging from their influence on the inward current induced by local application of the acetylcholine: the duration of the ACh current increases and its amplitude varies biphasically (a short-latency increase is succeeded by a decrease). Amiridin and tacrine intensify the extinction of the ACh current induced by repeated applications of ACh to the soma. The acetylcholinesterase inhibitor, physostigmine, exerts a similar modulatory influence on the ACh current and on its extinction, and also prevents the manifestation of the effects of amiridin and tacrine. Amiridin and physostigmine directly influence the cholinoreceptors and the ionic membrane channels controlled by them by similarly altering the voltage-current characteristics (VAC) of the ACh current, and by shifting the reversal potential of the ACh current in the negative direction, bringing it closer to the equilibrium potential for chloride ions; this may be interpreted as a result of the nonidentical action of these compounds on the various ionic currents controlled by cholinoreceptors. The hypothesis is advanced that the modulatory influence of amiridin, tacrine, and physostigmine on the activity and plasticity of the cholinoreceptors is governed by their direct membrane-cytoplasmic action.
运用记录普通蜗牛已识别的RPa3和LPa3神经元细胞内电位及跨膜电流的方法，研究了阿米立定和他克林对胆碱能受体膜电位、活性及可塑性的影响。阿米立定和他克林（1 - 100微摩尔/升）对细胞的膜电位没有明显影响。从它们对局部应用乙酰胆碱所诱发的内向电流的影响来看，这两种化合物都能调节胆碱能受体的活性：乙酰胆碱电流的持续时间增加，其幅度呈双相变化（先是短潜伏期增加，随后下降）。阿米立定和他克林增强了向细胞体重复施加乙酰胆碱所诱发的乙酰胆碱电流的消退。乙酰胆碱酯酶抑制剂毒扁豆碱对乙酰胆碱电流及其消退也有类似的调节作用，并且能阻止阿米立定和他克林作用的显现。阿米立定和毒扁豆碱通过类似地改变乙酰胆碱电流的电压 - 电流特性（VAC），以及使乙酰胆碱电流的反转电位向负方向移动，使其更接近氯离子的平衡电位，直接影响胆碱能受体及其控制的离子膜通道；这可以解释为这些化合物对胆碱能受体控制的各种离子电流的作用不同所致。有人提出假说，认为阿米立定、他克林和毒扁豆碱对胆碱能受体活性和可塑性的调节作用是由它们直接的膜 - 细胞质作用所决定的。
