Gamma-aminobutyric acid uptake is decreased in the hippocampus in a genetic model of human temporal lobe epilepsy.
Temporal lobe epilepsy (TLE) is one of the most commonly occurring and most intractable forms of seizure disorders in humans. The fundamental mechanisms underlying the pathogenesis of the disorder have, however, not yet been elucidated. El is an inbred mouse strain with genetic predisposition to epileptic seizures. The El mouse epilepsy shares its main features with TLE in humans and is considered to be an excellent model of the latter. We report a marked decrease in the uptake of gamma-aminobutyric acid (GABA) in the hippocampus of El mice. The data favor the involvement of GABA and the hippocampus in the mechanisms of TLE and suggest a genetic basis for the altered GABA uptake. This is the first report suggesting the possibility of a hereditary defect of a neurotransmitter function in TLE.
Janjua
N A
NA
Department of Neurochemistry, Okayama University Medical School, Japan.
Mori
A
A
Hiramatsu
M
M
D000818:Animals; D002540:Cerebral Cortex / Q000378:metabolism; D004195:Disease Models, Animal; D004833:Epilepsy, Temporal Lobe / Q000235:genetics* / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism*; D008297:Male; D051379:Mice; D008817:Mice, Mutant Strains; D010812:Physical Stimulation; D005680:gamma-Aminobutyric Acid / Q000493:pharmacokinetics*
D005680:gamma-Aminobutyric Acid