Abstract
β-Eudesmol, a sesquiterpenol extracted from a Chinese herb, Atractylodes lancea, at 10–80 μM, did not affect muscle action potentials, miniature and evoked endplate potentials and acetylcholine-induced depolarization in the presence or absence of neostigmine in mouse phrenic nerve-diaphragms. However, the tetanic fade, muscle fasciculation and twitch potentiation induced by neostigmine were effectively antagonized by 20 μM β-eudesmol. When trains of pulses were applied to the nerve in the presence of neostigmine, β-eudesmol reduced the incidence of explosive depolarization of the endplate from 95% to 35–67% of junctions, and shortened the duration when it occurred. Moreover, both the maximal and steady-state depolarizations during repetitive stimulation were reduced while the amplitudes of steady-state endplate potentials were increased. The results suggest that β-eudesmol antagonized neostigmine-induced neuromuscular failure mainly by a presynaptic action to depress the regenerative release of acetylcholine during repetitive stimulation. The mechanism of antagonism is obviously not tubocurarine-like and it is unrelated to desensitization of acetylcholine channels.
Published Version
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