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

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Abstract
1. Motor nerve terminals in magnesium‐poisoned rat hemidiaphragm‐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 no significant interaction between stimuli to the terminals at rates of 1 or 0·5/sec.2. Potassium‐free solutions at first increased, then decreased, the post‐tetanic depression of excitability. Raising [K]o threefold (15 m M) abolished the post‐tetanic depression and often converted it to an exaltation of excitability.3. Polarizing currents were applied to the terminals with a second electrode. Depolarizing currents increased, while hyperpolarizing currents decreased, the post‐tetanic depression of excitability.4. In solutions with 70% of the normal NaCl content replaced by sucrose, the post‐tetanic depression of excitability was reversibly prolonged.5. In the presence of 7·7 × 10−6 M digoxin or 0·42 m M ouabain there was a small reversible reduction of post‐tetanic excitability.6. After exposure to solutions containing no glucose or to solutions containing 3‐5 m M sodium azide the 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 × 10−6 M) had little or no effect upon post‐tetanic excitability.7. It was concluded that the post‐tetanic depression of excitability reflected hyperpolarization of the terminals and that this hyperpolarization was caused by a shift of the membrane potential towards the potassium equilibrium potential because of an increase in potassium permeability.