Abstract

Publisher Summary In this chapter, the factors determining the time course of end-plate currents (EPCs)— that is, activity of acetylcholinesterase (AChE), life-time of ionic channels, length of diffusional pathways, and repetitive binding of acetylcholine molecules, are discussed. It also discusses their importance in various neuromuscular junctions. M. sartorius and m. ileofibularis from the frog Rana temporariu and m. extensor digitorum longus and m. soleus from the rat were used. EPCs and miniature end-plate currents (MEPCs) were recorded in fast (m. sartorius, m. ileofibularis) and slow (m. ileofibularis) muscle fibres of the frog or in m. extensor digitorium longus, and m. soleus of the rat by the voltage clamp or focal extracellular recording techniques. The duration of EPC rise time and decay in frog fast junctions was quite different from that in the slow ones, and the difference remained after AChE inhibition. Atropine shortened the time course of EPCs more readily in fast junctions than in the slow ones. If AChE was inhibited, the iontophoretic application of tubocurarine also shortened the decay of MEPCs in fast junctions more than in the slow ones. EPC and MEPC decay remained to be exponential, with time constant dependent upon the membrane potential after AChE inhibition by reversible or irreversible inhibitors or by collagenase treatment. If AChE was inhibited, the substitution of sucrose or unpermeant Tris + ions for Na + resulted in prolongation of EPCs and MEPCs in both types of junctions, the effect being more pronounced at fast junctions.

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