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4‐AMINOPYRIDINE AND EVOKED TRANSMITTER RELEASE FROM MOTOR NERVE ENDINGS

1 In the presence of tetrodotoxin, electrotonic depolarization of frog motor nerve terminals causes the appearance of stimulus‐graded endplate potentials. When 4‐aminopyridine is added, the graded endplate potential is converted into a triggered all‐or‐none response resulting in giant endplate potentials of about 70 mV amplitude and 50 ms duration. The triggered endplate potentials are abolished in Ca2+ ‐free saline and are blocked by Mn2+ ions. Sr2+ but not Ba2+ can replace Ca2+ in supporting transmitter release. Mg2+ fails, even in concentrations as high as 32 mm, to affect the amplitude and the shape of the endplate potential but abolishes it when the Ca2+ concentration is reduced to 0.2 mm. 2 Despite the large amplitude of the triggered endplate potential in the presence of 4‐aminopyridine and tetrodotoxin, repetitive stimulation up to 10 Hz causes only a small decline in amplitude of successive endplate potentials. However, in the presence of (+)‐tubocurarine or gallamine, repetitive nerve stimulation produces a marked decline in successive endplate potential amplitude. The fall is counteracted when evoked transmitter release is reduced in the presence of 0.2 mm Ca2+. The results suggest that in the presence of 4‐aminopyridine such large amounts of transmitter are released that even during repetitive stimulation (5 to 10 Hz) endplate potentials are of maximal amplitude. 3 4‐Aminopyridine causes a parallel shift to the right of the dose‐response curve to Mg2+ for blockade of nerve impw/se‐evoked transmitter release (in the absence of tetrodotoxin). A similar parallel shift occurs in the presence of tetraethylammonium and guanidine. 4 It is concluded that 4‐aminopyridine increases transmitter release by enhancing the transport efficacy for Ca2+ across the nerve terminal membrane during nerve terminal depolarization.