Voltage dependencies of the effects of chlorpromazine on the nicotinic receptor channel from mouse muscle cell line So18

The effects of chlorpromazine (CPZ) on nicotinic acetylcholine receptor (nAChR) were re-investigated by patch-clamp recordings on a mouse muscle cell line: (1) CPZ decreased the channel-opening frequency and, thus, acted as a closed-channel blocker. This effect was independent of the membrane potential and was consistent with an enhanced desensitization of the nAChR. (2) In addition, CPZ decreased the mean channel open time of the nAChR in a concentration- and voltage-dependent manner and, thus, behaved as an open-channel blocker. The latter effect supports the notion that CPZ binds to a site within the nAChR ionic channel.