Swelling-induced release of glutamate, aspartate, and taurine from astrocyte cultures

• DOI: 10.1523/jneurosci.10-05-01583.1990
• Publication Date: 2018-03-30T14:15:33Z
• Authors: HK Kimelberg; SK Goderie; S Higman; S Pang; RA Waniewski
• Keywords: Anions; 0301 basic medicine; Aspartic Acid; Cell Survival; Cytochalasin B; Taurine; Sodium; Glutamic Acid; Biological Transport; Culture Media; 03 medical and health sciences; Glutamates; Hypotonic Solutions; Astrocytes; Animals; Amino Acids; Cells, Cultured

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.