抄録
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. β1 subunit plays critical roles in modulating the activation and inactivation kinetics of sodium current in epilepsy. 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 related to gene changes in VGSC. The present study was undertaken to detect sodium channel β1 subunit expression and mutation analysis in hippocampus of SERs. In this study, the mRNA expression of β1 subunit in SERs hippocampus was significantly higher than that in control Wistar rats hippocampus by RT-PCR; The protein expression of β1 subunit as measured with immunofluorescence and western blot was significantly increased; However, no sequence mutation was detected in five exons of β1 subunit by means of mutation analysis. Our study suggests for the first time that up-regulation of sodium channel β1 subunit at the mRNA and protein levels of SER hippocampus that underlies the observed seizure phenotype in SER might be a secondary appearance of the epileptiform activity instead of the causal role. [J Physiol Sci. 2008;58 Suppl:S129]
