Abstract
Nitric oxide (NO) content in rat cerebral cortex was measured using Electron Spin Resonance (ESR) spectroscopy. A nearly fivefold elevation in NO content was found at the peak time of pentylenetetrazole (PTZ)-induced seizures. The administration of N-nitro-L-arginine (L-NNA), a competitive inhibitor of NO-synthase, at the dose of 250 mg/kg, completely prevented the NO increase induced by PTZ, although clonic convulsions in the animals have been observed. L-NNA (10 mg/kg) was shown to delay the onset of clonic seizures as well as to shorten the latency of the first convulsive twitch. The level of lipid peroxidation secondary products measured as the content of thiobarbituric acid reactive species (TBARS) was increased in the cerebral cortex of PTZ-treated rats. L-NNA (250 mg/kg) failed to prevent the increased TBARS level produced by PTZ. The results support the notion that NO may play a trigger role in the pathophysiology of convulsive seizures.
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