Altered residual ATP content in rat brain cortex subcellular fractions following status epilepticus induced by lithium and pilocarpine.

Changes in residual ATP concentrations were investigated following subcellular fractionation of rat brain cortex after a prolonged period of status epilepticus induced by sequential administration of lithium and pilocarpine. After 2 h of continuous high-amplitude rapid spiking on EEG, we found significantly decreased levels of residual ATP in the homogenate and mitochondria fractions from status epilepticus rat brains compared to matched controls. No difference in residual ATP level was observed in the synaptosomal preparations of status epilepticus animals compared to controls. Inorganic phosphate concentration in the status animals was higher than controls in the cytosolic fraction only. F1-ATPase activity, an enzymatic indicator of mitochondrial ATP synthesis rate, was significantly higher in the status brains, whereas other mitochondrial enzymes were not different in the status and control rat groups. These findings, together with our earlier report of reduced synaptosomal ecto-ATPase activity, suggest that either the corresponding in vivo ATP concentrations were reduced as a result of status epilepticus or other biochemical changes had occurred that facilitated the hydrolysis of ATP following decapitation. Controls for and measurement of such other changes failed to provide an explanation for the observed changes in residual ATP.