title: Progressive metabolic changes underlying the chronic reorganization of brain circuits during the silent phase of the lithium-pilocarpine model of epilepsy in the immature and adult Rat.
abstract: The lithium-pilocarpine (Li-Pilo) model of epilepsy reproduces most of the features of human temporal lobe epilepsy. In the present study, we explored the correlation between metabolic changes, neuronal damage, and epileptogenesis during the silent phase following status epilepticus (SE) induced by Li-Pilo in 10- (P10) and 21-day-old (P21) and adult rats. Cerebral metabolic rates for glucose (CMR(glcs)) were measured at 14 and 60 days after SE by the 2-[(14)C]deoxyglucose method and neurodegeneration was assessed by the silver staining and cresyl violet techniques. In P10 rats, there was no damage and no metabolic consequences at any time after SE. In P21 rats, metabolic decreases were recorded at 14 days after SE, mainly in damaged forebrain regions. Conversely at 60 days after SE, P21 rats exhibited metabolic increases in both forebrain-damaged and brain-stem-intact areas. Finally, in adult rats studied at 14 days after SE, CMR(glcs) decreased in damaged forebrain areas involved in the circuitry of spontaneous seizures and increased in nondamaged brain-stem areas involved in the remote control of epilepsy. The increase in CMR(glcs) in damaged forebrain areas of P21 rats at 60 days after SE may reflect the genesis of a new circuitry underlying the occurrence of spontaneous seizures. The metabolic increase recorded in nondamaged brain-stem areas of P21 and adult rats occurs in regions involved in the remote control of seizures and might underlie a process of protection against the occurrence of seizures.
authors.affiliation: INSERM U398, Université Louis Pasteur, Strasbourg, 67085, France.
authors.forename: C
authors.initials: C
authors.lastname: Dubé
authors.forename: S
authors.initials: S
authors.lastname: Boyet
authors.forename: C
authors.initials: C
authors.lastname: Marescaux
authors.forename: A
authors.initials: A
authors.lastname: Nehlig
mesh_terms: D000367:Age Factors; D000818:Animals; D001522:Behavior, Animal; D048588:Benzoxazines; D001933:Brain Stem / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D002250:Carbon Radioisotopes; D016923:Cell Death / Q000502:physiology; D002540:Cerebral Cortex / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D004396:Coloring Agents; D003847:Deoxyglucose / Q000494:pharmacology; D004195:Disease Models, Animal; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005947:Glucose / Q000378:metabolism*; D008094:Lithium; D008297:Male; D018721:Muscarinic Agonists; D009410:Nerve Degeneration / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D009434:Neural Pathways; D010078:Oxazines; D010862:Pilocarpine; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D016622:Silver Staining; D013569:Synapses / Q000502:physiology; D013997:Time Factors
chemical_list: D048588:Benzoxazines; D002250:Carbon Radioisotopes; D004396:Coloring Agents; D018721:Muscarinic Agonists; D010078:Oxazines; D010862:Pilocarpine; C028911:cresyl violet; D008094:Lithium; D003847:Deoxyglucose; D005947:Glucose