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Enhanced Aspartate Release from Hippocampal Slices of Epileptic (El) Mice

Authors


  • The present address of Dr. A. Wieraszko is Department of Biology, CSI/IBR Center for Developmental Neuroscience, The City University of New York at the College of Staten Island, Staten Island, NY, 10301, U.S.A.

Address correspondence and reprint requests to Dr. T. N. Seyfried at Biology Department, Boston College, Chestnut Hill, MA 02167, U.S.A.

Abstract

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.

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