LACK OF INVOLVEMENT OF NITRIC-OXIDE IN THE MECHANISMS OF SEIZURES ANDHIPPOCAMPAL DAMAGE PRODUCED BY KAINATE AND OUABAIN IN RATS

The gross behavioural, electrocortical and neuropathological effects o f kainate (10 mg/kg i.p,) and ouabain (1 mu g, given into one dorsal h ippocampus) were studied in rats. The effects of these treatments on n itric oxide synthase (NOS) activity in homogenates of hippocampus and cortex were also studied. Administration of kainate or ouabain produce d motor and electrocortical seizures similar for latency to onset (app roximately 15 min) and intensity (in all instances 80-100% of the trea ted rats showed behavioural and electrographic seizures). These effect s were accompanied at 24 h by severe damage to all subsectors of the h ippocampal formation and this concerned a similar proportion of the tr eated rats (n = 4-8 per treatment). No significant changes in nitric o xide synthase (NOS) activity were noted in the cerebral cortex and hip pocampus of rats receiving injections of kainate and ouabain. In addit ion, pretreatment with N-omega-Nitro-L-arginine methyl ester (300 mu g , given into one lateral cerebral ventricle 15 min previously) was ine ffective in preventing the effects of kainate and ouabain. In conclusi on, present data suggest that excessive production of NO is not involv ed in the mechanisms triggering seizures and neurodegeneration produce d by kainate or ouabain.