Aspartic acid release from cerebral cortical slices of E1 mice with high seizure susceptibility.

Unlike their parent strain ddY mice, inbred mutant E1 mice are highly susceptible to convulsive seizures upon tossing stimulation. The uptake and release of [3H]aspartate by cerebral neocortical slices were investigated in non-stimulated E1 mice [E1(-)], in stimulated E1 mice [E1(+)] and also in ddY mice using a superfusion system. The uptake and release of aspartate in E1(-) were lower than in E1(+) or ddY. However, the aspartate level in the cerebral cortex of E1(-) was higher compared to that of E1(+) or ddY. Addition of aspartate into the medium resulted to a decreased potassium-stimulated aspartate release in ddY, an increased in E1(-), and no change in E1(+). The results suggest that abnormal state of aspartate release and/or uptake in cerebral cortex of E1 mice may contribute to their increased susceptibility of seizures.