Anticonvulsant effects of methyl ethyl ketone and diethyl ketone in several types of mouse seizure models

Nobuyoshi Hasebe, Kohji Abe, Eriko Sugiyama, Rie Hosoi, Osamu Inoue

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)


The anticonvulsant effects of acetone have been reported in various animal models of epilepsy. We recently demonstrated that other ketone bodies, methyl ethyl ketone (MEK) and diethyl ketone (DEK), suppressed status epilepticus that was induced by lithium-pilocarpine in rat. In the present study, the anticonvulsant effects of MEK and DEK were evaluated by using four different types of mouse seizure models, which were induced by pentylenetetrazole, kainic acid, methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate (DMCM), and electroshock. The effects of clonazepam, a typical anticonvulsant, and acetone were also evaluated and compared with MEK and DEK. In this study, MEK (5 and 10mmol/kg, i.p.) and DEK (2.5 and 5mmol/kg, i.p.) produced anticonvulsant activity against all types of seizure models. Furthermore, MEK and DEK showed almost the same potencies against four different seizure models used, while clonazepam showed significant higher ED50 values against kainic acid-induced and electroshock-induced seizure models as compared with the pentylenetetrazole- or DMCM-induced seizure model. In each study, the highest doses of clonazepam (1 or 3mg/kg) did not show clear anticonvulsant effects against the kainic acid- or electroshock-induced seizures. In conclusion, MEK and DEK showed broad-spectra anticonvulsant effects in both chemically- and electroshock-induced experimental seizure models.

Original languageEnglish
Pages (from-to)66-71
Number of pages6
JournalEuropean Journal of Pharmacology
Issue number1-3
Publication statusPublished - Sept 2010
Externally publishedYes


  • Anticonvulsant
  • Electroshock-induced convulsion
  • Kainic acid
  • Ketone body
  • Methyl-6,7-dimethoxy-4-ethyl-β-carboline-3-carboxylate
  • Pentylenetetrazole

ASJC Scopus subject areas

  • Pharmacology


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