Selective targeting of Scn8a prevents seizure development in a mouse model of mesial temporal lobe epilepsy

摘要: We previously found that genetic mutants with reduced expression or activity of Scn8a are resistant to induced seizures and co-segregation a mutant allele can increase survival seizure resistance Scn1a mice. In contrast, is increased in the hippocampus following status epilepticus amygdala kindling. These findings point as promising therapeutic target for epilepsy raise possibility aberrant overexpression limbic structures may contribute some epilepsies, including temporal lobe epilepsy. Using small-hairpin-interfering RNA directed against gene, we selectively intrahippocampal kainic acid (KA) mouse model mesial knockdown prevented development spontaneous 9/10 mice, ameliorated KA-induced hyperactivity, reactive gliosis. results support potential targeting treatment refractory