Kimelberg H K, Cheema M, O'Connor E R, Tong H, Goderie S K, Rossman P A
Division of Neurosurgery, Albany Medical College, New York 12208.
J Neurochem. 1993 May;60(5):1682-9. doi: 10.1111/j.1471-4159.1993.tb13391.x.
Exposure of primary astrocyte cultures to isosmotic ethanol from 10-100 mM led to both swelling of the cells and release of [3H]taurine and D-[3H]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 hypoosmotic 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.