Changes in (14)C-labeled 2-deoxyglucose brain uptake from nickel-induced epileptic activity

Unilateral epidural applications of nickel solution to motor cortex were followed in about 1 h by contralateral forelimb myoclonus. In rats which displayed frequent myoclonal jerking during the 45-min 2-deoxyglucose (2-DG) uptake and clearing period, autoradiographic analysis showed that glucose utilization at the nickel implant site was greater in the supragranular and infragranular layers than in the granular layer (in normal cortex, activity is greatest in the granular layer), and was also greater in the substantia nigra and other subcortical centers. The same cortical and most of the subcortical changes in 2-DG uptake were also observed when metabolic activity was assessed 1 h after myoclonus had stopped, indicating that it may not have been the seizure activity itself that had altered metabolic activity, but some process engendered by the seizures - possibly a tissue response to excitotoxic damage. In fact, rats which displayed infrequent myoclonus showed negligible increases in cortical and subcortical uptake. These results do not support an earlier claim that increased glucose consumption is the metabolic signature of the interictal activity produced by seizure-inducing metals. Indeed, the findings raise the possibility that tissue damage is responsible for interictal hypermetabolism when it is observed in animal models of epilepsy.