PT  - JOURNAL ARTICLE
AU  - HK Kimelberg
AU  - SK Goderie
AU  - S Higman
AU  - S Pang
AU  - RA Waniewski
TI  - Swelling-induced release of glutamate, aspartate, and taurine from astrocyte cultures
AID  - 10.1523/JNEUROSCI.10-05-01583.1990
DP  - 1990 May 01
TA  - The Journal of Neuroscience
PG  - 1583--1591
VI  - 10
IP  - 5
4099  - http://www.jneurosci.org/content/10/5/1583.short
4100  - http://www.jneurosci.org/content/10/5/1583.full
SO  - J. Neurosci.1990 May 01; 10
AB  - 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.