Reduced local input to fast-spiking interneurons in the somatosensory cortex in the GABA(A) gamma 2 R43Q mouse model of absence epilepsy

摘要

ObjectiveAbsence seizures in childhood absence epilepsy are initiated in the thalamocortical (TC) system. We investigated if these seizures result from altered development of the TC system before the appearance of seizures in mice containing a point mutation in -aminobutyric acid A (GABA(A)) receptor 2 subunits linked to childhood absence epilepsy (R43Q). Findings from conditional mutant mice indicate that expression of normal 2 subunits during preseizure ages protect from later seizures. This indicates that altered development in the presence of the R43Q mutation is a key contributor to the R43Q phenotype. We sought to identify the cellular processes affected by the R43Q mutation during these preseizure ages.