[End plate currents with a physiological level of quantal secretion and after potentiation of the mediator release by 4-aminopyridine]

Abstract

The role of postsynaptic potentiation (PSP) and asynchronous secretion of acetylcholine (ACh) in generation of multiquantal and plate currents (EPC) was studied under voltage clamp conditions in the cut sartorius muscle of frog before and after 4-aminopyridine (4-AP) treatment. If compared with miniature EPC (MEPC), multiquantal EPC had larger amplitude and more prolonged both rise-time and decay. In the presence of 4-AP the difference between the decay time constant of EPC (tau epc) and MEPC (tau mepc) became much more pronounced. Mean quantal content of EPC was 249 in control 373 and 423 in the presence of 1 X 10(-5) and 1 X 10(-4) mol/l of 4-AP, respectively. Magnesium ions (6-10 mmol/l) reduced the amplitude and tau epc of EPC without affecting its rise-time. Repetitive activity (10 Hz, 60s) resulted in the reduced amplitude and tau epc but in increased rise-time of EPC. D-tubocurarine (5 X 10(-7) mol/l) and alpha-bungarotoxin (1 X 10(-6) g/ml) diminished the difference between tau epc and tau mepc. In the presence of 4-AP all these effects were much more pronounced. It was suggested that asynchronous secretion of ACh from motor nerve terminals caused prolongation of the rise-time, reduction in the amplitude of EPC, but had little or no effect on the decay rate of EPC. The slow decay of multiquantal EPC both in the absence and in the presence of 4-AP was almost entirely due to postsynaptic interaction of ACh quanta, i. e. PSP.