Wickenden Alan D
Icagen Inc, Suite 460, 4222 Emperor Boulevard, Durham, NC 27703, USA.
Neuropharmacology. 2002 Dec;43(7):1055-60. doi: 10.1016/s0028-3908(02)00237-x.
It is estimated that up to 30% of epilepsy patients are poorly treated with available anti-epileptic drugs (AEDs). Thus, there is a medical need for new AEDs with novel mechanisms of action to serve as alternate or adjunct therapy for the treatment of drug-resistant or refractory epilepsy. One potential anti-epileptic mechanism that has not yet been exploited is K(+) channel opening. Considerable genetic, molecular, physiological and pharmacological evidence now exists to support a role for K(+) channels such as KCNQ2/Q3, Kv1.1, KATP and GIRK2 in the control of neuronal excitability and epileptogenesis. Evidence supporting these K(+) channels as novel AED targets will be reviewed in the following article.
据估计,高达30%的癫痫患者使用现有的抗癫痫药物(AEDs)治疗效果不佳。因此,医学上需要具有新型作用机制的新型AEDs,作为耐药性或难治性癫痫治疗的替代或辅助疗法。一种尚未被利用的潜在抗癫痫机制是钾(K+)通道开放。现在有大量的遗传学、分子学、生理学和药理学证据支持KCNQ2/Q3、Kv1.1、KATP和GIRK2等K+通道在控制神经元兴奋性和癫痫发生中的作用。支持这些K+通道作为新型AED靶点的证据将在以下文章中进行综述。