Systemically administered cycloheximide reduces inhibition in rat neocortical slice preparation.
Global cerebral ischemia leads to long lasting hyperexcitability and a reduced protein synthesis in non-infarcted tissue surrounding the lesion. In this study we investigated whether protein synthesis inhibition by pharmacological means itself changes neocortical excitability. Two hours after the last of three i.p. injections with the protein synthesis inhibitor cycloheximide (12 h interval, 1.5 mg/kg body weight) we observed a widespread reduction of neocortical inhibition. The study indicates that inhibition of protein synthesis may contribute to the altered brain excitability following ischemia.
Buchkremer-Ratzmann
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Neurologische Klinik, Heinrich-Heine-Universität, Düsseldorf, Germany.
Witte
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D000818:Animals; D002545:Brain Ischemia / Q000378:metabolism*; D002540:Cerebral Cortex / Q000187:drug effects*; D003513:Cycloheximide / Q000494:pharmacology*; D004353:Drug Evaluation, Preclinical; D004558:Electric Stimulation; D005071:Evoked Potentials / Q000187:drug effects; D066298:In Vitro Techniques; D007274:Injections, Intraperitoneal; D008297:Male; D009433:Neural Inhibition / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects*; D014176:Protein Biosynthesis / Q000187:drug effects; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar
D011500:Protein Synthesis Inhibitors; D003513:Cycloheximide