Abstract
The age-related functional changes underlying epileptogenesis remain to be clarified. In the present study, we explored the correlation between metabolic changes, neuronal damage and epileptogenesis during the acute, silent and chronic phases following status epilepticus (SE) induced by lithium-pilocarpine (Li-Pilo) in 10- (P10), 21-day-old (P21) and adult rats. Local cerebral metabolic rates for glucose (LCMR<sub>glcs</sub>) were measured by the [<sup>14</sup>C]2-deoxyglucose method during SE, the silent period and the interictal phase of the chronic period. Neurodegeneration was assessed by cresyl violet staining. During SE, LCMR<sub>glcs</sub> dramatically increased at all ages mainly in forebrain vulnerable regions. During the silent phase, in P21 and adult rats, metabolic decreases were recorded in damaged forebrain regions involved in the genesis and propagation of seizures 14 days after SE. At the end of the silent phase, P21 and adult rats exhibited metabolic increases in intact brainstem areas involved in the remote control of epilepsy. During the interictal phase of the chronic period, LCMR<sub>glcs</sub> decreased in damaged forebrain areas of adult and P21 rats that were not spontaneously epileptic, while LCMR<sub>glcs</sub> were similar to control levels in epileptic P21 rats. In P10 rats, there was no damage and no metabolic consequences at any time after SE. In conclusion, the process of epileptogenesis and its functional consequences differ in P21 and adult rats. The factors underlying these age-related differences remain to be explored.
Published Version
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