Involvement of Na+/Ca2+ Exchanger in Pentylenetetrazol-Induced Convulsion by Use of Na+/Ca2+ Exchanger Knockout Mice

Involvement of Na+/Ca2+ exchanger (NCX) in pentylenetetrazol (PTZ)-induced convulsion by use of NCX knockout mice and the selective ligand SEA0400 to NCX was examined. In the SEA0400-administered group, the latency to clonic convulsion was extended into 210 s, although the latency to clonic convulsion was observed until 100 s in control group. SEA0400 had little effect on bicuculline-induced clonic seizure nicotine-induced wild running and 4-aminopyridine-induced tonic flexion, respectively. Tonic flexion convulsion was occurred three fifth in the wild type mice group by administration of PTZ, but tonic flexion was not observed in NCX1 knockout mice groups. These results suggest that NCX is involved in inhibitory action in PTZ-induced convulsion. Epilepsy is a common psychiatric disorder, and in the last decade, genetic abnormalities of genes encoding ion channels expressed in the brain have been identified as the cause of twenty idiopathic epilepsy syndromes. We have already reported that nicotinic acetylcholine receptor mutation exhibit the nocturnal frontal lobe epilepsy phenotype in rats.1)