An investigation of the post-tetanic potentiation of end-plate potentials at a mammalian neuromuscular junction

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Abstract
End-plate potentials (e.p.p.s) were recorded intracellularly from neuromuscular junctions in curarized or Mg-paralyzed rat diaphragm-phrenic nerve preparations in vitro. In Mg-paralyzed preparations after 1000 impulses at 100/sec the amplitude of e.p.s elicited at 1/sec before and after the tetanus was on average greater than the control amplitude for 120 + 30 sec. The post-tetanic potentiation (P.T.P.) of e.p.p. amplitudes was not thought to be dependent upon post-tetanic hyperpolarization (P.T.H.) of nerve terminals as it lasted longer than the hyperpolarization generated by an identical tetanus; was unaffected by hyperpolarizing currents which reduced P.T.H. or depolarizing currents which prolonged P.T.H.; and was diminished in solutions containing 30% of the normal NaCl [sodium chloride] concentration or 1% ethyl alcohol, both of which procedures prolong P.T.H. The magnitude and duration of P.T.P. we re influenced by the pH of the bath ing solution in the range 7- 7.5 although there was no change in P.T.H. under these conditions. The inability of polarizing currents to influence P.T.P. was also thought inconsistent with the hypothesis that P.T.P. is due toan increase inavailable transmitter. P.T. P. was not thought to be due to sodium accumulation in nerve terminals, for P.T.P. was reduced or abolished by procedures which would be expected to increase the intraterminal sodium ion concentration. These procedures were: exhibitionof metabolic inhibitors (1.810" 6 [image] antimycin A, 3-5 m[image] sodium azide or 1 mMsodium iodoacetate), exhibition of cardiac glycosides(7.7x10-6 [image]digoxin or 0.42 m[image] ouabain), and omission of glucose or potassium ions from the bathing solution. Abolition of P.T.P. by potassium-free solutions was also thought to be inconsistent with the hypothesis that P.T.P. is due to a reduction in the potassium concentration in nerve terminals. P.T.P. was not thought to be due to terminal volume changes, for no consistent effect upon the quantal content of e.p.p.s could be detected in hypo- or hy-perosmotic solutions. The only hypothesis for P.T.P. not excluded by our experiments was that P.T.P. is due to some change in ionized calcium at a membrane site important in transmitter release.