Overview
- Ashoor, A. et al. (2011) Eur. J. Pharmacol. 673, 26.
Alomone Labs Chlorpromazine hydrochloride reversibly inhibits nicotinic receptors heterologously expressed in Xenopus oocytes.A. Time course of the inhibitory effect of 10 µM Chlorpromazine hydrochloride (#C-165) on α7 nicotinic currents, elicited at -80 mV holding potential by continuous stimulation with 100 µM ACh + 3 µM PNU 282987 (#P-110) every 50 sec (indicated by uppermost horizontal bars). B. Superimposed traces of channel activity before and during application of the indicated Chlorpromazine concentration (taken from the experiment shown in panel A).
Phenothiazines (PTZs) are a family of compounds commonly used in the treatment of psychiatric disorders. The mechanism whereby these drugs exert their therapeutic effects appears to be through the blockade of dopamine receptors1.
These substances have also been shown to affect a number of other physiologically important sites. PTZs also compete for serotonin and α-adrenergic and histamine receptors2. Electrophysiological studies have shown that PTZs interfere with a number of ligand- and voltage-activated channels3.
Chlorpromazine (CPZ) is a widely used PTZ. CPZ has been reported to strongly affect GABA-mediated inhibitory synaptic transmission by decreasing the amplitude and accelerating the decay of miniature IPSCs (mIPSCs)4. A recent study showed that CPZ decreased the channel-opening frequency of nicotinic acetylcholine receptors (nAChR) and thus, acted as a closed-channel blocker (IC50s values are ~10 µM)5.
