| Literature DB >> 12504910 |
Abstract
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.Entities:
Mesh:
Substances:
Year: 2002 PMID: 12504910 DOI: 10.1016/s0028-3908(02)00237-x
Source DB: PubMed Journal: Neuropharmacology ISSN: 0028-3908 Impact factor: 5.250