ENHANCED ASPARTATE RELEASE RELATED TO EPILEPSY IN (EL) MICE

Previous studies have shown that potassium-evoked, calcium-dependent, endogenous aspartate release is greater from hippocampal slices of adu lt epileptic (EL) mice than from nonepileptic control C57BL/6J (B6) mi ce. To examine further the association between epilepsy and enhanced a spartate release in EL mice, endogenous neurotransmitter release from hippocampal slices was studied in young, seizure-free EL mice and in t wo nonseizure control mouse strains, DDY and B6. DDY is the parental s train from which EL arose, and it has a genetic background similar to EL. Released amino acid neurotransmitters were quantitated by HPLC wit h fluorescent detection and were expressed as picomoles of amino acid released per minute of incubation per slice +/- SEM. Aspartate release was significantly higher in EL mice (15.8 +/- 0.8) than in either the control B6 or DDY mice (8.5 +/- 1.4 and 8.4 +/- 1.7, respectively). N o significant differences were found among the B6, DDY, and EL mice fo r the release of glutamate (23.0 +/- 2.0, 32.3 +/- 5.8, and 25.9 +/- 2 .6, respectively) or GABA (23.5 +/- 0.7, 19.5 +/- 3.2, and 21.8 +/- 3. 2, respectively). Thus, enhanced aspartate release precedes the onset of EL seizures and may be related to the cause rather than to the effe cts of seizure activity.