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Hydrogen sulfide (H<jats:sub>2<\/jats:sub>S) is a gas transmitter that may mediate cerebral ischemic injury. But the role of H<jats:sub>2<\/jats:sub>S in seizures has not been understood yet. We examined the effect of H<jats:sub>2<\/jats:sub>S on seizure\u2010like events (<jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>s) and underlying mechanisms.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods and Results<\/jats:title><jats:p>Pentylenetetrazole (<jats:styled-content style=\"fixed-case\">PTZ<\/jats:styled-content>)\u2010 and pilocarpine\u2010induced rat epileptic seizure models were tested. Low\u2010Mg<jats:sup>2+<\/jats:sup>\/high\u2010K<jats:sup>+<\/jats:sup>\u2010 and 4\u2010aminopyridine (4\u2010<jats:styled-content style=\"fixed-case\">AP<\/jats:styled-content>)\u2010induced epileptic seizure models were examined using patch\u2010clamp recordings in brain slices. It was found that Na<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> aggravated both <jats:styled-content style=\"fixed-case\">PTZ<\/jats:styled-content>\u2010 and pilocarpine\u2010induced <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>s in rats, while both low\u2010Mg<jats:sup>2+<\/jats:sup>\/high\u2010K<jats:sup>+<\/jats:sup>\u2010 and 4\u2010<jats:styled-content style=\"fixed-case\">AP<\/jats:styled-content>\u2010induced <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>s were also exacerbated by Na<jats:styled-content style=\"fixed-case\">HS<\/jats:styled-content> in brain slices, which may be due to its regulation on the voltage\u2010gated sodium channel, N\u2010methyl\u2010D\u2010aspartic acid receptor (<jats:styled-content style=\"fixed-case\">NMDAR<\/jats:styled-content>), and <jats:italic>\u03b1<\/jats:italic>\u2010amino\u20103\u2010hydroxy\u20105\u2010methyl\u20104\u2010isoxazolepropionic acid receptor (<jats:styled-content style=\"fixed-case\">AMPAR<\/jats:styled-content>) function. Furthermore, these effects were reversed by blocking voltage\u2010gated sodium channel, <jats:styled-content style=\"fixed-case\">NMDAR<\/jats:styled-content>, and <jats:styled-content style=\"fixed-case\">AMPAR<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These results suggest a pathological role of increased H<jats:sub>2<\/jats:sub>S level in <jats:styled-content style=\"fixed-case\">SLE<\/jats:styled-content>s <jats:italic>in vivo<\/jats:italic> and in <jats:italic>vitro<\/jats:italic>. Enzymes that control H<jats:sub>2<\/jats:sub>S biosynthesis could be interesting targets for antiepileptic strategies in poststroke epilepsy treatment.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.12228","type":"journal-article","created":{"date-parts":[[2014,1,31]],"date-time":"2014-01-31T06:30:44Z","timestamp":1391149844000},"page":"411-419","source":"Crossref","is-referenced-by-count":38,"title":["Aggravation of Seizure\u2010like Events by Hydrogen Sulfide: Involvement of Multiple Targets that Control Neuronal Excitability"],"prefix":"10.1111","volume":"20","author":[{"given":"Yi","family":"Luo","sequence":"first","affiliation":[{"name":"Department of Pharmacology Tongji Medical College Huazhong University of Science and Technology Wuhan China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peng\u2010Fei","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Pharmacology Tongji Medical College Huazhong University of Science and Technology Wuhan 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