The　spontaneously　epileptic　rat　(SER),　a　double　mutant　(zi/zi,　tm/tm),　exhibits　both　tonic　convulsions　and　absence-like　seizures　from　the　age　of　8　weeks.　Since　the　first　point　mutation　in　the　voltage-gated　sodium　channel　(VGSC)　β1　subunit　in　human　generalized　epilepsy　with　febrile　seizures　plus　(GEFS+)　was　identified,　more　and　more　types　of　genetic　epilepsy　have　been　causally　suggested　to　be　related　to　gene　changes　in　VGSC.　However,　there　are　no　reports　that　can　elucidate　the　effects　of　VGSC　in　SER.　The　present　study　was　undertaken　to　detect　sodium　channel　I　α-isoform　(Nav1.1),　sodium　channel　III　α-isoform　(Nav1.3)　and　β1　subunit　from　both　the　level　of　mRNA　and　protein　in　SERs　hippocampus　compared　with　control　Wistar　rats.　In　this　study,　the　mRNA　expressions　of　Nav1.1,　Nav1.3　and　β1　subunit　in　SERs　hippocampus　were　significantly　higher　than　those　in　control　rats　hippocampus　by　real-time　RT-PCR;　The　protein　distributions　and　expressions　of　Nav1.1,　Nav1.3　and　β1　subunit　in　SERs　hippocampus　were　detected　by　immunofluorescence,　immunohistochemistry　and　western　blot,　and　the　protein　expressions　of　Nav1.1,　Nav1.3　and　β1　subunit　were　significantly　increased.　In　conclusion,　our　study　suggested　for　the　first　time　that　sodium　channel　Nav1.1,　Nav1.3　and　β1　subunit　up-regulation　at　the　mRNA　and　protein　levels　of　SER　hippocampus　might　contribute　to　the　generation　of　epileptiform　activity　and　underlie　the　observed　seizure　phenotype　in　SER.　The　results　of　this　study　may　be　of　value　in　revealing　components　of　the　molecular　mechanisms　of　hippocampal　excitation　that　are　related　to　genetic　epilepsy.　©　2007.