Sodium valproate and brainstem energetics.
The effect of the anticonvulsant sodium valproate on cerebral brainstem energy metabolism has been investigated. Stupor and coma were produced in mice by the intraperitoneal injection of sodium valproate at a dose of 600 mg/kg. Glucose, glycogen, ATP, and phosphocreatine were measured in small tissue samples from the ascending reticular activating system. Levels of all metabolites were either normal or elevated in precoma and comatose mice as compared to controls. These data are consistent with the concept that sodium valproate does not have a primary action through depletion of high energy phosphates.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001933:Brain Stem / Q000378:metabolism*; D003128:Coma / Q000139:chemically induced; D004734:Energy Metabolism / Q000187:drug effects*; D005260:Female; D005947:Glucose / Q000378:metabolism; D006003:Glycogen / Q000378:metabolism; D051379:Mice; D010725:Phosphocreatine / Q000378:metabolism; D012154:Reticular Formation / Q000378:metabolism; D014635:Valproic Acid / Q000494:pharmacology* / Q000633:toxicity
D010725:Phosphocreatine; D014635:Valproic Acid; D000255:Adenosine Triphosphate; D006003:Glycogen; D005947:Glucose