Abstract
Antipsychotic drugs are thought to exert their therapeutic action by antagonizing dopamine receptors but are also known to produce side effects in the heart by inhibiting cardiac ether-a-go-go-related gene (ERG) K(+) channels. Recently, it has been discovered that the same channels are present in the brain, including midbrain dopamine neurons. ERG channels are most active after the cessation of intense electrical activity, and blockade of these channels prolongs plateau potentials in bursting dopamine neurons. This change in excitability would be expected to alter dopamine release. Therefore, the therapeutic action of antipsychotic drugs may depend on inhibition of both postsynaptic dopamine receptors and presynaptic ERG K(+) channels.
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