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Ethanol‐Induced Aspartate and Taurine Release from Primary Astrocyte Cultures
Author(s) -
Kimelberg H. K.,
Cheema M.,
O'Connor E. R.,
Tong H.,
Goderie S. K.,
Rossman P. A.
Publication year - 1993
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1993.tb13391.x
Subject(s) - taurine , astrocyte , swelling , ethanol , chemistry , tonicity , extracellular , potassium , biochemistry , osmotic concentration , calcium , biophysics , amino acid , biology , endocrinology , central nervous system , medicine , organic chemistry , pathology
Exposure of primary astrocyte cultures to isosmo‐tic ethanol from 10‐100 mA/ led to both swelling of the cells and release of [ 3 H]taurine and r[ 3 H]aspartate. Exposure to hyperosmotic ethanol, in the same concentration range. caused neither swelling nor release. Release was inhibited by the anion transport blocker L‐644,711, already shown to inhibit amino acid release evoked by hyposmotic or high‐potassium medium, conditions that also cause astrocytic swelling. Ethanol‐induced release generally showed a decline in response to successive exposures to ethanol, and release was not dependent on extracellular calcium. Thus, the characteristics of swelling‐induced release of amino acids by isosmotic ethanol seem to correspond to those of swelling‐induced release from astrocytes due to exposure to hypotonic or high‐K + media. We discuss whether such effects may contribute to CNS damage after head injury and stroke.