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Journal of Neuroscience, Vol 10, 1583-1591, Copyright © 1990 by Society for Neuroscience
Swelling-induced release of glutamate, aspartate, and taurine from astrocyte cultures
HK Kimelberg, SK Goderie, S Higman, S Pang and RA Waniewski
Division of Neurosurgery, Albany Medical College, New York 12208.
Swelling of primary astrocyte cultures by exposing them to hypotonic media
caused release of label after the cells had been allowed to accumulate
3H-L-glutamate, 3H-D-aspartate, or 3H-taurine. Comparable release of
endogenous L-glutamate or taurine, as measured by high- pressure liquid
chromatography (HPLC), was also found. Release of label was not affected by
treating the cells with cytochalasin B, indicating that microfilament
polymerization was not significantly involved. Hypotonic-induced release
did not appear to principally involve reversal of the Na(+)-dependent
uptake system since increasing external K+ to depolarize the cells by
replacement of external Na+, thus maintaining isotonic conditions,
increased release to a lesser extent. Threo beta-hydroxyaspartate, a potent
3H-L-glutamate uptake blocker, added externally stimulated efflux of
3H-L-glutamate independently of the swelling-induced efflux. Upon
restoration of swollen cells to isotonic medium they showed an unimpaired
ability to take up 3H-L- glutamate. The swelling-induced release of label
was inhibited by a number of anion transport inhibitors, one of which has
been shown to significantly improve outcome in an experimental brain
trauma/hypoxia model in which astrocyte swelling is an early event.
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