Topic: carbamazepine

Seizure-like activity (SLA) results from synchronous neuronal activity in the mouse hippocampal subregions, namely: CA1, CA3 and DG. While many studies have proved the anticonvulsant properties of the administration of anti-epileptic drugs, such as diazepam (DZP), a GABA-A receptor agonist, and carbamazepine (CBZ), a sodium channel blocker, their role in modulating the oscillatory patterns within these three regions remains unclear. Furthermore, the role of oscillatory dynamics in the pre-ictal period in predicting the emergence of a seizure events require further investigation. In our study,

Mutations in TMEM151A, an almost unknown gene, have been recently found in Paroxysmal Kinesigenic Dyskinesia (PKD), an autosomal dominant movement disorder and in few cases of Benign Familial Infantile Epilepsy (BFIE). The major gene associated to PKD and BFIE is PRRT2. Interestingly, the drug treatment of choice for PKD caused by TMEM151A or PRRT2 mutations is Carbamazepine, a sodium channel blocker. Indeed, PRRT2 has been shown to control neuronal excitability by modulating voltage gated sodium channels. Both PRRT2 and TMEM151A are membrane associated proteins expressed in the nervous system