Abstract
The neuromuscular blockade produced by succinylcholine (SuCh) is potentiated by β-eudesmol, a sesquiterpenoid alcohol isolated from Atractylodes lancea. β-Eudesmol blocks the nicotinic acetycholine receptor (nAChR) channel in both open and closed conformations. To clarify the mechanism of potentiation, we investigated the blocking effect of SuCh (0.1–10 μM) with β-eudesmol on nAChR channel activity using the cell-attached patch clamp technique. Pretreatment with β-eudesmol (20 μM) affected neither resting membrane potential nor ACh-activated channel activities. β-Eudesmol produced the following changes in ACh-activated channel currents modulated by SuCh: reduction of SuCh (above 0.3 μM)-induced prolongation of channel open time and decrease in the frequency of channel opening in the presence of SuCh (above 3 μM). These results suggest that the potentiating effect of β-eudesmol is postsynaptically due to accelarated desensitization of the nAChR, presumably resulting from preferential blocking action during the closed state of the receptor channel.
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