青蛙肌肉中重复终板活动和单终板电流期间脱敏作用的发展。

Development of desensitization during repetitive end-plate activity and single end-plate currents in frog muscle.

Giniatullin R A, Khamitov G, Khazipov R, Magazanik L G, Nikolsky E E, Snetkov V A, Vyskocil F

Kazan Medical Institute, USSR.

J Physiol. 1989 May;412:113-22. doi: 10.1113/jphysiol.1989.sp017606.

Abstract

The amplitudes of end-plate currents (EPCs) in short trains of fifteen to seventeen EPCs at 10 Hz were depressed in the presence of 10 microM-proadifen when acetylcholinesterase (AChE) was inhibited. 2. The proadifen-induced EPC depression was voltage-dependent and the effect was more pronounced at negative membrane potentials. 3. In the presence of proadifen, the mean amplitude of miniature end-plate currents (MEPCs) was reduced by 36% 5 s after the EPC train as compared with MEPCs before the train. 4. Without proadifen, but with inhibited AChE, an increase of temperature from 20 to 26 degrees C and elevation of external Ca2+ from 1.8 to 2.5 mM led to EPC amplitude depression in the train, which was also potential-dependent. 5. After AChE inhibition, proadifen (10 microM) progressively shortened MEPC decay without significant reduction of amplitude up to 40 min of exposition. MEPCs were not affected by proadifen when AChE was active. 6. It is concluded that these postsynaptic effects of proadifen can be explained neither by its action on the resting acetylcholine receptors (AChR) nor on open ion channels but are due to its desensitization-promoting action.

摘要

当乙酰胆碱酯酶（AChE）被抑制时，在10赫兹下15至17个终板电流（EPC）的短串刺激中，终板电流的幅度在10微摩尔普罗地芬存在的情况下降低。2. 普罗地芬诱导的EPC降低是电压依赖性的，并且在负膜电位时效应更明显。3. 在普罗地芬存在下，与串刺激前的微小终板电流（MEPC）相比，EPC串刺激后5秒，微小终板电流的平均幅度降低了36%。4. 没有普罗地芬但AChE被抑制时，温度从20摄氏度升高到26摄氏度以及细胞外Ca2+从1.8毫摩尔升高到2.5毫摩尔会导致串刺激中EPC幅度降低，这也是电位依赖性的。5. AChE抑制后，普罗地芬（1 microM）在长达40分钟的暴露时间内逐渐缩短MEPC衰减，而幅度没有显著降低。当AChE活跃时，MEPC不受普罗地芬影响。6. 得出的结论是，普罗地芬的这些突触后效应既不能通过其对静息乙酰胆碱受体（AChR）的作用来解释，也不能通过其对开放离子通道的作用来解释，而是由于其促进脱敏的作用。