Abstract
Rationale) Seizure susceptibility and epileptogenesis depend not only on protein associated with glutamatergic and/or GABAergic neuronal transmission, but also on the redox. In glutamate transporter knockout (GLAST KO) mice, the kindling phenomena in GLAST KO developed more slowly while the after discharge duration (ADD) was briefer than that of the control C57BL-6J mice. To explain these phenomena, we focused the hippocampal redox state in the GLAST KO mice. Matreial and Methods) To measure anti-oxidant ability, the elimination of nitroxide radical was measured by usage of microdialysis combined with X-band ESR spectroscopy. Resluts) Nitroxide radical in the dialysate was eliminated exponentially, which means endogenous anti-oxidant reduced the paramagnetism of nitroxide radical. Half-life in GLAST KO. Discussion) Kindling-induced after discharge in electroencepharograms depends on the protein associated with glutamatergic and/or GABAergic neuronal transmission. But, there was no alteration except for increased GAT-3 expression, which supports enhanced GABAergic inhibition. In addition to enhanced GABAergic inhibition, Ca++ influx necessary for kindling development would be suppressed by oxidized redox state. From these physiological background, kindling development of GLAST KO mice was slower rather than taht of control. [J Physiol Sci. 2007;57 Suppl:S115]
