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Although previous studies have suggested that nitric oxide (NO) plays a role in the neurotoxicity of MMA, the involvement of NO\u2010induced nitrosative damage from inducible nitric oxide synthase (iNOS) in MMA\u2010induced seizures are poorly understood. In the present study, we showed a decrease of time spent convulsing induced by intracerebroventricular administration of MMA (2 \u03bcmol\/2 \u03bcL; i.c.v.) in iNOS knockout (iNOS<jats:sup>\u2212\/\u2212<\/jats:sup>) mice when compared with wild\u2010type (iNOS<jats:sup>+\/+<\/jats:sup>) littermates. Visual analysis of electroencephalographic recordings (EEG) showed that MMA injection induced the appearance of high\u2010voltage synchronic spike activity in the ipsilateral cortex which spreads to the contralateral cortex while quantitative electroencephalographic analysis showed larger wave amplitude during MMA\u2010induced seizures in wild\u2010type mice when compared with iNOS knockout mice. We also report that administration of MMA increases NOx (NO<jats:sub>2<\/jats:sub> plus NO<jats:sub>3<\/jats:sub> content) and 3\u2010nitrotyrosine (3\u2010NT) levels in a greater extend in iNOS<jats:sup>+\/+<\/jats:sup> mice than in iNOS<jats:sup>\u2212\/\u2212<\/jats:sup> mice, indicating that NO overproduction and NO\u2010mediated damage to proteins are attenuated in iNOS knockout mice. In addition, the MMA\u2010induced decrease in Na<jats:sup>+<\/jats:sup>, K<jats:sup>+<\/jats:sup>\u2010ATPase activity, but not in succinate dehydrogenase (SDH) activity, was less pronounced in iNOS<jats:sup>\u2212\/\u2212<\/jats:sup> when compared with iNOS<jats:sup>+\/+<\/jats:sup> mice. These results reinforce the assumption that metabolic collapse contributes for the secondary toxicity elicited by MMA and suggest that oxidative attack by NO derived from iNOS on selected target such as Na<jats:sup>+<\/jats:sup>, K<jats:sup>+<\/jats:sup>\u2010ATPase enzyme might represent an important role in this excitotoxicity induced by MMA. Therefore, these results may be of value in understating the pathophysiology of the neurological features observed in patients with methylmalonic acidemia and in the development of new strategies for treatment of these patients.<\/jats:p><\/jats:sec>","DOI":"10.1016\/j.ijdevneu.2008.11.005","type":"journal-article","created":{"date-parts":[[2008,11,28]],"date-time":"2008-11-28T10:37:35Z","timestamp":1227868655000},"page":"157-163","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Methylmalonate\u2010induced seizures are attenuated in inducible nitric oxide synthase knockout mice"],"prefix":"10.1002","volume":"27","author":[{"given":"Leandro Rodrigo","family":"Ribeiro","sequence":"first","affiliation":[{"name":"Centro de Ci\u00eancias da Sa\u00fade Laborat\u00f3rio de Psicofarmacologia e Neurotoxicidade, Departamento de Fisiologia e Farmacologia Universidade Federal de Santa Maria Santa Maria RS 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