Absence seizures are believed to be elicited by T-type calcium channels in the thalamic reticular nucleus of the brain that regulate influxes of calcium. These channels enable thalamic reticular nucleus neurons to generate burst firing, leading the neurons to enter a hyper-excited state.
In order to identify the relationship between burst firing and absence seizures, the researchers conducted an experiment to induce absence seizures in mice using gene targeting techniques to delete the T-type calcium channel CaV3.3. The results showed that mice that received a complete genetic deletion of the T-type calcium channel, which in turn suppressed burst firing in the thalamic reticular nucleus, exhibited an increased frequency of absence seizures.
Moreover, the researchers observed for the first time ever that tonic firing also increased in such mice. The study was the first to discover that tonic firing plays a key role in the induction of absence seizure, which contradicts the existing hypothesis and carries significant implications for absence seizure treatment research.
The study is meaningful in respect to the fact that it calls into question the role of the T-type calcium channel in the reticular thalamus, and is expected to provide an important theoretical foundation for understanding its role in the mechanism of absence seizures, as well as developing effective treatment methods for absence epilepsy.