S Kaneko, K Kurahashi, S Fujita, Y Fukushima, T Sato, R G Hill
{"title":"Potentiation of GABA by midazolam and its therapeutic effect against status epilepticus.","authors":"S Kaneko, K Kurahashi, S Fujita, Y Fukushima, T Sato, R G Hill","doi":"10.1111/j.1440-1819.1983.tb00338.x","DOIUrl":null,"url":null,"abstract":"<p><p>The anticonvulsive effect of midazolam was studied in rats and mice brains. Microiontophoretically applied midazolam (0.2M, pH 3.5) potentiated the GABA effect at the single neurone level, and inhibited neuronal firing in the rat cuneate neurones. Midazolam administered intraperitoneally (15 mg/kg) increased the primary afferent depolarization for at least two hours. Three mg/kg of midazolam slightly increased the glutamate decarboxylase activities in the mice cerebrum and the increase was statistically significant (p less than 0.05). The authors reported a case of clinical application of midazolam: a status epilepticus was successfully treated with it, while intravenous diazepam of 30 mg failed to control the status.</p>","PeriodicalId":75857,"journal":{"name":"Folia psychiatrica et neurologica japonica","volume":"37 3","pages":"307-9"},"PeriodicalIF":0.0000,"publicationDate":"1983-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1111/j.1440-1819.1983.tb00338.x","citationCount":"16","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Folia psychiatrica et neurologica japonica","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1111/j.1440-1819.1983.tb00338.x","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 16
Abstract
The anticonvulsive effect of midazolam was studied in rats and mice brains. Microiontophoretically applied midazolam (0.2M, pH 3.5) potentiated the GABA effect at the single neurone level, and inhibited neuronal firing in the rat cuneate neurones. Midazolam administered intraperitoneally (15 mg/kg) increased the primary afferent depolarization for at least two hours. Three mg/kg of midazolam slightly increased the glutamate decarboxylase activities in the mice cerebrum and the increase was statistically significant (p less than 0.05). The authors reported a case of clinical application of midazolam: a status epilepticus was successfully treated with it, while intravenous diazepam of 30 mg failed to control the status.