Interneuron FGF13 regulates seizure susceptibility via a sodium channel-independent mechanism (Updated August 19, 2024).

A recent preprint abstract discusses the role of FGF13, a protein involved in the regulation of seizures. The study found that mutations in FGF13 can lead to developmental and epileptic encephalopathies (DEEs), which are neurological disorders characterized by recurrent seizures. The researchers used cell type-specific knockout mice to investigate the effects of FGF13 deletion in different types of neurons. They discovered that deleting FGF13 in interneurons led to seizures and imbalanced inhibitory/excitatory activity in the brain, while deleting it in excitatory neurons had no detectable effects. Interestingly, the study found that FGF13 does not regulate sodium channels as previously thought, but instead affects potassium channel currents. These findings contribute to our understanding of the molecular mechanisms underlying FGF13-related seizures and expand our knowledge of FGF13 functions in different types of neurons. It is important to note that this preprint has not yet undergone peer review. [Extracted from the article]