Abstract
The role of postysynaptic potentiation (PSP) and asynchronous secretion of acetylcholine (ACh) in the generation of multiquantal currents and end plate currents (EPC) was investigated under voltage clamp conditions in transected sartorius muscle of the frog before and after 4-aminopyridine (4-AP) treatment. Compared with miniature EPC (MEPC), showing an average quantum content of 249, multiquantal EPC has a larger amplitude, longer rise-time, and longer decay-time (τepc). Magnesium ions (6–10 mM) reduce the amplitude and τspec of EPC without affecting its rise-time. Rhythmical stimulation (10 Hz for 60 sec) results in reduced amplitude and τ but increased rise-time of EPC. D-turbocurarine (5×10−7 M) and α-bungarotoxin (1×10−5 gm/ml) diminishes the difference between τepc and τmepc. In the presence of 4-AP, all these effects are much more pronounced. It is proposed that asynchronous secretion of ACh from motor nerve teminals causes prolongation of the rise-time and reduction of the amplitude of EPC but has little or no effect upon the decay rate of EPC. The slow decay of multiquantal EPC, both in the absence and in the presence of 4-AP, is almost entirely due to postynaptic interaction of ACh quanta, i.e., PSP.
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Kurashov Meidcal Institute, Kazhan. Translated from Neirofiziologiya, Vol. 23, No. 1, pp. 48–56, January–February, 1991.
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Giniatullin, R.A., Khazipov, R.N. End plate currents at the physiological level of quantal secretion and after potentiation of transmitter release by 4-aminopyridine. Neurophysiology 23, 40–47 (1991). https://doi.org/10.1007/BF01052288
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DOI: https://doi.org/10.1007/BF01052288