• Epilepsy;
  • Epileptic (El) mice;
  • Hippocampal slices;
  • Potassium depolarization;
  • Exicitatory amino acid release

Abstract: The release of putative neurotransmitters [aspartate, glutamate, and γ-aminobutyric acid (GABA)] was studied in hippocampal slices from adult normal C57BL/6J (B6) and El (epileptic) mice. The El mice, a genetic model of temporal lobe epilepsy, had an average of 86 seizures. Sets of B6 and El hippocampal slices (400 μm thick) were incubated in a series of normal and high potassium (60 mM) buffers in the presence or absence of calcium. The calcium-dependent and calcium-independent potassium-induced release of amino acids was compared in each mouse strain. Release of endogenous amino acids was measured using liquid chromatog-raphy with electrochemical detection and was expressed as picomoles of amino acid released per milliliter of incubation buffer per minute of incubation per slice ± SEM. No significant differences were found between the El and B6 mice for the calcium-dependent potassium-evoked release of glutamate (18.20 ± 2.62 and 15.41 ± 3.56), or GABA (17.28 ± 2.90 and 12.73 ± 1.37), respectively. Aspartate release, however, was significantly higher in the El mice (6.62 ± 0.69) than in the B6 mice (3.31 ± 0.72). These findings suggest that enhanced aspartate release may be related to seizure expression in El mice.