Abstract
Lamotrigine is an antiepileptic drug employed in the treatment of partial epilepsies. We studied its possible interaction with channels other than its known therapeutic target, the voltage-gated sodium channel, using the adult muscle nicotinic acetylcholine receptor as a model system. At the single-channel level, lamotrigine caused a dose-dependent (a) diminution in mean open time, (b) increase in mean burst duration and (c) increase in the area of a new closed-time component. A simple linear channel blocking mechanism accounts for these results. Thus, lamotrigine exerts a blocking action on the muscle nicotinic acetylcholine receptor.
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