ArticleProceedings of the National Academy of Sciences of the United States of America2025
Actions of the antiseizure drug carbamazepine in the thalamic reticular nucleus: Potential mechanism of aggravating absence seizures.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- The Thalamic Reticular Ultimatum: Carbamazepine's Betrayal in Absence Epileptic Seizures.Neuroscience bulletin · 2026Article
- Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism.Science advances · 2025Article
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Abstract
Carbamazepine (CBZ) is a widely used antiepileptic drug effective in managing partial and generalized tonic-clonic seizures. Despite its established therapeutic efficacy, CBZ has been reported to worsen seizures in another form of epilepsy, generalized absence seizures, in both clinical and experimental settings. In this study, we focused on thalamic reticular (RT) neurons, which regulate thalamocortical network activity in absence seizures, to investigate whether CBZ alters their excitability, thereby contributing to the exacerbation of seizures. Using ex vivo whole-cell patch-clamp electrophysiology, we found that CBZ selectively inhibits the tonic firing of RT neurons in a dose-dependent manner without affecting burst firing. At the RT-thalamocortical synapse, CBZ significantly increases the failure rate of GABAergic synaptic transmission, with greater effects on somatostatin-than parvalbumin-expressing RT neurons. In vivo EEG recordings and open-field behavior in Scn8a
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