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Astrocytic glutamate uptake and prion protein expression
Author(s) -
Brown David R.,
Mohn Christiane M.
Publication year - 1999
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/(sici)1098-1136(19990201)25:3<282::aid-glia8>3.0.co;2-n
Subject(s) - glutamate receptor , biology , astrocyte , extracellular , neuroglia , neurodegeneration , microbiology and biotechnology , cell culture , glutamic acid , biochemistry , neuroscience , amino acid , central nervous system , medicine , receptor , genetics , disease
Factors influencing glutamate uptake by astrocytes may indirectly influence neuronal survival. Elevated extracellular glutamate may be excitotoxic or may exacerbate neurodegeneration in various neurological diseases. By using a cell culture model, we have investigated the influence of astrocytic prion protein (PrP c ) expression on glutamate uptake. Type 1 astrocytes expressing PrP c have a higher rate of Na + ‐dependent glutamate uptake than PrP c ‐deficient type 1 astrocytes. This difference is exacerbated when serum free media is used to culture the astrocytes. Further analysis suggested that a decrease in substrate affinity is responsible for the sensitivity of PrP‐deficient astrocytic glutamate uptake to culture conditions. PrP c has been shown to bind copper. Greater sensitivity of cells to copper concentrations may be responsible for the decreased substrate affinity observed. PrP c ‐deficient cerebellar cells are more sensitive to glutamate toxicity in the presence of copper. These results show that glutamate uptake from astrocytes is dependent on PrP c expression which in turn may be related to copper metabolism. GLIA 25:282–292, 1999. © 1999 Wiley‐Liss, Inc.