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    Epilepsy Res. 2006 Aug;70 Suppl 1:S218-22. Epub 2006 Jun 27.

    Na channel gene mutations in epilepsy--the functional consequences.

    Source

    Laboratory for Neurogenetics, RIKEN Brain Science Institute, Hirosawa 2-1, Wako-shi, Saitama 351-0198, Japan. yamakawa@brain.riken.jp

    Abstract

    Mutations of voltage-gated sodium channel genes SCN1A, SCN2A, and SCN1B have been identified in several types of epilepsies including generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy in infancy (SMEI). In both SCN1A and SCN2A, missense mutations tend to result in benign idiopathic epilepsy, whereas truncation mutations lead to severe and intractable epilepsy. However, the results obtained by the biophysical analyses using cultured cell systems still remain elusive. Now studies in animal models harboring sodium channel gene mutations should be eagerly pursued.

    PMID:
    16806834
    [PubMed - indexed for MEDLINE]

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