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A Metabolic and Neuropathological Approach to the Understanding of Plastic Changes That Occur in the Immature and Adult Rat Brain During Lithium‐Pilocarpine–Induced Epileptogenesis
Author(s) -
Dubé Céline,
Marescaux Christian,
Nehlig Astrid
Publication year - 2000
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1157.2000.tb01554.x
Subject(s) - pilocarpine , epileptogenesis , lithium (medication) , neuroscience , status epilepticus , epilepsy , medicine , psychology , endocrinology
Summary:Purpose : The age‐related functional changes that underlie epileptogenesis remain to be clarified. In the present study, we explored the correlation between metabolic changes, neuronal damage, and epileptogenesis during the silent and chronic phases after status epilepticus (SE) induced by lithium‐pilocarpine in 10‐day‐old (P10), 21‐day‐old (P21), and adult rats. Methods : Local cerebral metabolic rates for glucose (LCMR glcs ) were measured by the [ 14 C]2‐deoxyglucose method during the silent period (14 and 60 days after SE in P10 and P21 rats and only at 14 days after SE in adult rats because the silent phase lasts for about 14 days in adults and 60 days in P21 rats) and the interictal phase of the chronic period (2 months after spontaneous seizures or 6 to 7 months after SE in P10 and P21 rats that do not become epileptic). Neurodegeneration was assessed by the silver staining and cresyl violet techniques. Results : In P10 rats, there was no damage and no metabolic consequences at any time after SE. During the silent phase in P21 rats, metabolic decreases were recorded at 14 days after SE, mainly in damaged forebrain regions. At 60 days after SE, P21 rats exhibited metabolic increases in both damaged forebrain and intact brainstem areas. In adult rats studied at 14 days after SE, LCMR glcs decreased in damaged forebrain areas involved in the genesis and propagation of seizures and increased in brainstem areas involved in the remote control of epilepsy. During the interictal phase of the chronic period, LCMR glcs decreased in damaged forebrain areas of adult epileptic rats and P21 rats that were not spontaneously epileptic, whereas it was similar to control levels in epileptic P21 rats. Conclusions : The process of epileptogenesis and its effects differ in duration and functional consequences in P21 and adult rats. The factors that underlie these age‐related differences remain to be explored.