title: Mapping of cerebral energy metabolism in rats with genetic generalized nonconvulsive epilepsy.
abstract: The quantitative 2-[14C]deoxyglucose autoradiographic method was applied to measure local cerebral metabolic rates of glucose (LCMRglc) in a model of genetic petit-mal-like seizures in a strain of Wistar rats. During the experimental period, epileptic rats exhibited synchronous spike-and-wave discharges, whereas the EEG pattern of control animals was normal. Overall, LCMRglc was consistently higher in epileptic rats than in the non-epileptic controls. The increase in LCMRglc was widespread and concerned all cerebral functional systems studied, whether they exhibit spike-and-wave discharges (neocortex and thalamus), or not (limbic system). These results are in good accordance with positron-emission tomography measurements in humans with typical childhood absence epilepsy. There appears to be a lack of anatomical correlation between areas demonstrating hypermetabolism and areas where spike-and-wave discharges are recorded. The administration of 200 mg/kg ethosuximide completely suppressed spike-and-wave discharges in epileptic rats and did not change the EEG pattern in controls. However, LCMRglc were increased to the same extent over control values in epileptic rats whether they were injected with ethosuximide or untreated. By contrast, when epileptic rats were given 2 mg/kg haloperidol, the frequency and the length of spike-and-wave discharges increased, inducing almost a permanent petit-mal status epilepticus. Haloperidol did not change EEG pattern in controls. In haloperidol-treated epileptic rats, LCMRglc decreased to levels comparable to those measured in untreated control rats. In the presence of haloperidol, LCMRglc were similar in both control and epileptic rats. Thus, the diffuse increase in cerebral energy metabolism in epileptic rats as compared to controls is not directly related to the occurrence of spike-and-wave discharges, and may rather be associated with inhibitory mechanisms involved in their termination and suppression, as well as their spread to limbic and motor structures.
authors.affiliation: INSERM U272, Université de Nancy I, France.
authors.forename: A
authors.initials: A
authors.lastname: Nehlig
authors.forename: M
authors.initials: M
authors.lastname: Vergnes
authors.forename: C
authors.initials: C
authors.lastname: Marescaux
authors.forename: S
authors.initials: S
authors.lastname: Boyet
mesh_terms: D000818:Animals; D001921:Brain / Q000378:metabolism*; D001931:Brain Mapping / Q000379:methods; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000187:drug effects; D004734:Energy Metabolism / Q000502:physiology*; D004832:Epilepsy, Absence / Q000378:metabolism*; D005013:Ethosuximide; D005947:Glucose / Q000378:metabolism*; D006220:Haloperidol; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains / Q000235:genetics; D012016:Reference Values
chemical_list: D005013:Ethosuximide; D005947:Glucose; D006220:Haloperidol