Abstracts

Epileptogenesis is associated with collapse of glutamate regulation, alteration in redox state and generation of free radicals. However, measurement of reductants in brain tissue extracts is problematic because of intrinsic free radical scavenging. Using in vivo methods, we measured hippocampal antioxidant ability from the decay rate of i.p injection of nitroxide radical with 700 MHz Electron Paramagnetic Resonance (EPR) spectroscopy during amygdalar ferric chloride-induced chronic recurrent seizures in rats., We used Region-Selected Intensity Determination (RSID) methods for estimation of nitroxide decay ratio. Hippocampal antioxidant function was estimated based on the half-life of the EPR signal of the blood-brain barrier-permeable nitroxide radical. Rats underwent unilateral right amygdalar injection with aqueous ferric chloride. Recording from chronically implanted depth electrodes showed development of epileptiform discharges, followed by recurrent seizures arising from amygdalar regions with propagation into both hippocampi. EPR spectroscopy with RSID estimation was performed at 5 days, 15 days and 30 days after FeCl[sub]3[/sub] injection., In bilateral dorsal hippocampal regions, in vivo antioxidant ability was significantly decreased at 5 days and 30 days in animals with chronic, recurrent seizures when compared to controls., We observed impairment of antioxidant function in the hippocampi of rats with epileptogenesis induced by amygdalar ferric chloride injection. Of interest, unilateral induction of a chronic seizure focus was associated with bilateral alterations both early after injection and late. We wonder if hippocampal collapse of glutamate regulation during epileptogenesis might be followed by consumption of endogenous antioxidants., (Supported by: Grant-in-Aid for Scientific Research (C)(2)(16591146) from the Ministry of Education, Science, Sport and Culture, Japan (to Y.U.).)