The origin of the post‐tetanic hyperpolarization of mammalian motor nerve terminals

Abstract

Motor nerve terminals in magnesium-poisoned rat heroidiaphragm-phrenic nerve preparations in vitro were stimulated with short depolarizing pulses of approximately threshold strength and the evoked antidromic responses recorded from the phrenic nerve. The percentage of these 1/sec or 0.5/sec stimuli to which there was no antidromic response was used as a quantitative measure of the terminal excitability. After standard tetanic stimulation (1000 impulses at 100/sec) the excitability of the terminals was depressed for an average duration of 60-70 sec, during most of which time no antidromic responses to stimuli of pretetanic intensity were recorded. There was nosignificant interaction between stimuli to the terminals at rates of 1 or 0.5/sec. Potassium-free solutions at first increased, then decreased, the post-tetanic depression of excitability. Raising [K]o threefold (15 m[image]) abolished the post-tetanic depression and often converted it to an exaltation of excitability. Polarizing currents were applied to the terminals with a 2nd electrode. Depolarizing currents increased, while hyperpolarizing currents decreased, the post-tetanic depression of excitability. In solutions with 70% of the normal NaCl [sodiumchloride] content replaced by sucrose, the post-tetanic depression of excitability was reversibly prolonged. In the presence of 7.7 xl0-6 [image]digoxin or 0.42m[image] ouabain there was a small reversible reduction of post-tetanic excitability. After exposure to solutions containing no glucose or to solutions containing 3-5 in[image] sodium azidethe excitability of the terminals was not altered by the tetanus. After washing with the control solution, post-tetanic depression of excitability returned. Antimycin-A (1.8 x 10-6 [image]) had little or no effect upon post-tetanic excitability. The post-tetanic depression of excitability reflected hyperpolarization of the terminals and this hyperpolarization was caused by a shift of the membrane potential towards the potassium equilibrium potential becauseof an increase in potassium permeability.