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Sodium‐dependent glutamate uptake as an activator of oxidative metabolism in primary astrocyte cultures from newborn rat
Author(s) -
Eriksson Gun,
Peterson Anders,
Iverfeldt Kerstin,
Walum Erik
Publication year - 1995
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.440150207
Subject(s) - glutamate receptor , kainate receptor , biology , metabotropic glutamate receptor , nmda receptor , ampa receptor , ouabain , astrocyte , agonist , biochemistry , medicine , sodium , biophysics , endocrinology , receptor , chemistry , central nervous system , organic chemistry
In the present report we describe the effect of glutamate on respiratory activity in primary cultures of astrocytes, derived from cerebral cortex of newborn rat. Glutamate (100 μM) caused an increased oxygen consumption. This effect could not be inhibited by antagonists to the NMDA or AMPA/kainate receptors. Neither trans‐ACPD (an agonist to the metabotropic glutamate receptor) nor the Krebs cycle intermediate α‐ketoglutarate had any effect on the respiratory rate. An uncontrolled influx of Na + , caused by gramicidin, could mimic the glutamate effect on respiratory activity. In addition, the glutamate effect was abolished by addition of ouabain or replacement of Na + by Li + in the perfusion buffer. We conclude that the co‐transport of Na + , in the Na + ‐dependent high‐affinity glutamate uptake system, mediated the glutamate‐induced increase in oxygen consumption through an increased activity of Na + /K + ‐ATPases. © 1995 Wiley‐Liss, Inc.