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  • Title: Sequential changes of nitric oxide levels in the temporal lobes of kainic acid-treated mice following application of nitric oxide synthase inhibitors and phenobarbital.
    Author: Kato N, Sato S, Yokoyama H, Kayama T, Yoshimura T.
    Journal: Epilepsy Res; 2005 Jun; 65(1-2):81-91. PubMed ID: 15979286.
    Abstract:
    Although studies have indicated a close relationship between nitric oxide (NO) and kainic acid (KA)-induced seizures, the role of NO in seizures is not fully understood. Here, we quantified NO levels in the brain of KA-treated mice using EPR spectrometry to elucidate the role of NO in KA-induced seizures. KA was administered to mice with or without pretreatment with one of the following: N(G)-nitro-l-arginine methyl ester (l-NAME), an NO synthase (NOS) inhibitor that acts on both endothelial NOS (eNOS) and neuronal NOS (nNOS); 7-nitroindazole (7-NI), which acts more selectively on nNOS in vivo; or the anti-epileptic drug, phenobarbital. To accurately assess NO production during seizure activity, we directly measured KA-induced NO levels in the temporal lobe using an electron paramagnetic resonance NO trapping technique. Our results revealed that the both dose- and time-dependent changes of NO levels in the temporal lobe of KA-treated mice were closely related to the development of seizure activity. l-NAME mediated suppression of the KA-induced NO generation led to enhanced severity of KA-induced seizures. In contrast, 7-NI induced only about 50% suppression and had little effect on seizure severity; while phenobarbital markedly reduced both NO production and seizure severity. These results show that KA-induced neuroexcitation leads to profound increases in NO release to the temporal lobe of KA-treated mice and that NO generation from eNOS exerts an anti-convulsant effect.
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