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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机译：人们认为抗精神病药通过拮抗多巴胺受体发挥其治疗作用，但也已知通过抑制心脏随动相关基因（ERG）K +通道在心脏产生副作用。最近，已经发现大脑中存在相同的通道，包括中脑多巴胺神经元。在强烈的电活动停止后，ERG通道最活跃，对这些通道的阻断延长了爆发多巴胺神经元的平台电位。这种兴奋性的变化有望改变多巴胺的释放。因此，抗精神病药的治疗作用可能取决于抑制突触后多巴胺受体和突触前ERG K +通道。
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