| pubmed-article:6722542 | pubmed:abstractText | Measurement of regional brain glucose metabolism may give information concerning the mechanism of neuronal cell death developing after prolonged periods of epileptic activity. Regional brain glucose utilization was measured in paralyzed ventilated rats during seizures induced by L-allylglycine, kainic acid and bicuculline using the [14C]deoxyglucose method. Regional brain glucose concentration was measured in another series of rats, after similar periods of seizure activity, to permit a more accurate calculation of the lumped constant. In L-allylglycine-induced seizures regional brain glucose concentration did not vary from control values, so no correction of the lumped constant was necessary. Regional brain glucose utilization increased throughout the brain, the largest increase being in the hippocampus (control 36 +/- 6 mumol 100 g-1 min-1; seizure 120 +/- 12 mumol 100 g-1 min-1). In kainic acid-induced seizures, brain glucose concentration fell in the hippocampus, involving some correction of the lumped constant. Increases in glucose utilization were limited primarily to the hippocampus, with some involvement of the inferior colliculus. The ventral hippocampus showed the largest increase in glucose utilization (control 34 +/- 5 mumol 100 g-1 min-1; seizure 167 +/- 10 mumol 100 g-1 min-1). In bicuculline-induced seizures, in starved rats, brain glucose concentration fell in all regions investigated and no increase in regional glucose utilization was recorded. In L-allylglycine and kainic acid-induced seizures, the hippocampus, a region vulnerable to neuronal damage, shows the largest increase in glucose utilization. Studies involving bicuculline need further investigation, due to severe perturbation of brain and plasma glucose concentration. | lld:pubmed |
