Abstract
Less than 4% of miniature end-plate potentials (MEPPs) in frog cutaneous-pectoral muscles, normal or exposed to nonimmune rabbit serum were atypical. These MEPPs were of normal amplitude, but their time course was nearly twice as slow as that of normal MEPPs. The exposure of muscles to rabbit anti-galactocerebroside serum induced more than three-fold increase in the fraction of atypically slow MEPPs. Inhibition of acetylcholinesterase caused an appearance of giant MEPPs, the fraction of slow MEPPs being unchanged. Possible mechanisms of increase in fraction of atypical slow MEPPs based on modification of the synaptic Schwann cell functioning are discussed.
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