Abstract
Endplate potentials (epps) were recorded intracellularly from single diaphragm fibers, in vitro, of newborn (≤ 10 days, n = 10) and older (18–29 days, n = 5) rats with glass microelectrodes. The muscle was stimulated via the phrenic nerve for 1 s at 10, 20 or 50 Hz. Muscle action potentials were blocked by μ conotoxin GIIIA, a specific muscle Na + channel blocker. In diaphragms from older animals, epps followed nerve stimulation at the 3 frequencies, with a gradual decrement in amplitude to 70% of the first epp at 50 Hz. The younger age group showed an initial enhancement of epp amplitude, followed by large variability in amplitude. These data suggest that neuromuscular transmission failure in the newborn diaphragm is secondary to variability in neurotransmitter release as compared to the more mature diaphragm.
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