{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T18:56:20Z","timestamp":1780080980436,"version":"3.54.0"},"reference-count":53,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2009,1,29]],"date-time":"2009-01-29T00:00:00Z","timestamp":1233187200000},"content-version":"vor","delay-in-days":212,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2008,7]]},"abstract":"<jats:p><jats:bold>Background and purpose:<\/jats:bold> The sodium channel is a primary target for treating central nervous system disorders such as epilepsy. In this study the anticonvulsant effect of BmK IT2, a sodium channel\u2010specific neurotoxin, was evaluated in different animal models of epilepsy.<\/jats:p><jats:p><jats:bold>Experimental approach:<\/jats:bold> Experiments were performed on freely moving rats made epileptic by administration of either pentylenetetrazole (PTZ) or pilocarpine. BmK IT2 (0.05\u20130.5\u2003\u03bcg in 2\u2003\u03bcl) was microinjected into the CA1 area and its effects on PTZ\u2010induced widespread, seizure\u2010like behaviour and cortex epileptiform EEG, as well as on pilocarpine\u2010induced seizure\u2010like behaviour and c\u2010Fos expression were studied.<\/jats:p><jats:p><jats:bold>Key results:<\/jats:bold> Intrahippocampal application of BmK IT2 dose\u2010dependently inhibited PTZ\u2010induced seizure\u2010like behaviour, and reduced the numbers and duration of the high amplitude and frequency discharges (HAFDs) of the epileptiform EEG component induced by PTZ. Similarly, in the pilocarpine\u2010induced status epilepticus (SE) model, BmK IT2 significantly prolonged the latency to onset of the SE, reduced the severity of SE and suppressed hippocampal c\u2010Fos expression during SE.<\/jats:p><jats:p><jats:bold>Conclusions and implications:<\/jats:bold> BmK IT2 showed anticonvulsant activity as it inhibited the widespread seizures induced by PTZ and pilocarpine\u2010induced SE in rats. This activity might be due to the modulation of sodium channels in the hippocampus. Hence, BmK IT2 could be used as a novel tool to explore the molecular and pathological mechanisms of epilepsy with regard to the involvement of sodium channels.<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2008) <jats:bold>154<\/jats:bold>, 1116\u20131124; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/bjp.2008.156\">10.1038\/bjp.2008.156<\/jats:ext-link>; published online 21 April 2008<\/jats:p>","DOI":"10.1038\/bjp.2008.156","type":"journal-article","created":{"date-parts":[[2008,6,30]],"date-time":"2008-06-30T11:27:31Z","timestamp":1214825251000},"page":"1116-1124","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":30,"title":["Anticonvulsant effect of BmK IT2, a sodium channel\u2010specific neurotoxin, in rat models of 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