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Glutamate receptor agonists up-regulate glutamate transporter GLAST in astrocytes

1996; Lippincott Williams & Wilkins; Volume: 8; Issue: 1 Linguagem: Inglês

10.1097/00001756-199612200-00052

1473-558X

Georgi Gegelashvili, Gianluca Civenni, Giorgio Racagni, Niels C. Danbolt, Inger Schousboe, Arne Schousboe,

Amino Acid Enzymes and Metabolism

LONG-TERM treatment of astrocytes in primary culture with L-glutamate (0.1–3 mM) resulted in a dose-dependent increase in D-[3H]aspartate uptake. The effect was abolished by an antagonist of kainate/AMPA receptors, CNQX, and mimicked by kainate, but not by AMPA or tACPD. Both glutamate and kainate caused a dramatic up-regulation (82% and 69%, respectively) of GLAST, a predominant glutamate transporter in cultured astroglia, though the mRNA levels appeared unaffected. Long-term treatment of cultures with dBcAMP stimulated D-[3H]aspartate uptake as well as GLAST expression. Apart from glutamate, none of the agonists used was capable of increasing further the uptake capacity of the dBcAMP-treated astroglia. The glutamate receptor- dependent modulation of glutamate transport in astroglial cultures may represent a novel feedback regulatory mechanism for glutamate uptake in the brain.