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L‐glutamate‐stimulated taurine release from rat cerebral cultured astrocytes
Author(s) -
Koyama Y.,
Ishibashi T.,
Tanaka K.,
Baba A.
Publication year - 1994
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.490380110
Subject(s) - taurine , glutamate receptor , kainate receptor , astrocyte , extracellular , osmotic concentration , biochemistry , chemistry , biology , medicine , endocrinology , central nervous system , amino acid , ampa receptor , receptor
We characterized L‐glutamate‐stimulated taurine release from cultured astrocytes prepared from rat cerebrum. L‐glutamate (0.5 mM) stimulated release of 3 H‐labeled and endogenous taurine, where the rate of release reached maximum in 40 min. L‐glutamate increased astrocytic volume [ 3 H‐O‐methyl‐D‐glucose ( 3 H‐OMG) space] with a similar time course to 3 H‐taurine release. Quisqualate, L‐aspartate, DL‐homocysteate, and L‐cysteate increased both astrocytic 3 H‐OMG space and 3 H‐taurine release from cultured astrocytes, while kainate (1 mM) stimulated 3 H‐taurine release without affecting astrocytic volume. N‐methyl‐D‐aspartate had no effect on 3 H‐taurine release and astrocytic volume. Treatment of astrocytes with dibutyryl cAMP reduced the effect of kainate on 3 H‐taurine release. L‐glutamate‐stimulated 3 H‐taurine release was attenuated by removal of extracellular Cl − and in hyperosmotic medium, which prevented L‐glutamate‐induced increase in 3 H‐OMG space of cultured astrocytes. These results indicate that L‐glutamate stimulates taurine release from astrocytes through swelling‐triggered mechanisms and that kainate causes the release through volume‐independent mechanisms. © 1994 Wiley‐Liss, Inc.