SCN8A and juvenile absence epilepsy: Similarly, recent research using two different models of genetic generalized epilepsy with absence seizures (WAG/Rij rats and Scn8a+/mut mice, a mutant model harboring a loss-of-function SCN8A mutation) showed that oligodendrogenesis and myelination specifically increased within the thalamo-cortical network involved in seizure generation following seizure onset [179].