摘要
When teaching neurology students about epilepsy,selecting appropriate antiseizure medications(ASMs)based on seizure type is a fundamental objective.Carbamazepine(CBZ),a widely used first-line ASM,is effective against focal seizures,generalized tonic-clonic seizures,and mixed seizure patterns[1].However,CBZ paradoxically aggravates absence seizures,as demonstrated by increased 36 Hz spike-and-wave discharges(SWDs)in both patients and animal models[2,3].While prior studies implicated altered GABAA receptor function in the thalamic ventrobasal complex[4],the precise mechanisms remained unclear.Recently,an inspiring study published on PNAS by Jang et al.from Stanford University has highlighted the thalamic reticular nucleus(RT)as the key brain region responsible for CBZ's aggravating effect on absence seizures[5].The combination of transgenic mouse models,optogenetics,and detailed electrophysiology in the original study provided exceptional precision in probing mechanistic insights,which greatly strengthens the conclusions.
基金
supported by the National Natural Science Foundation of China(82173796)
the Research Project of Zhejiang Chinese Medical University(2023JKZDZC04).
