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Pyroglutamate stimulates Na + ‐dependent glutamate transport across the blood–brain barrier
Author(s) -
Hawkins Richard A.,
Simpson Ian A.,
Mokashi Ashwini,
Viña Juan R.
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.06.097
Subject(s) - glutamate receptor , blood–brain barrier , transporter , membrane , intracellular , glutamate aspartate transporter , chemistry , biophysics , biochemistry , excitatory amino acid transporter , microbiology and biotechnology , biology , neuroscience , central nervous system , gene , receptor
Regulation of Na + ‐dependent glutamate transport was studied in isolated luminal and abluminal plasma membranes derived from the bovine blood–brain barrier. Abluminal membranes have Na + ‐dependent glutamate transporters while luminal membranes have facilitative transporters. This organization allows glutamate to be actively removed from brain. γ‐Glutamyl transpeptidase, the first enzyme of the γ‐glutamyl cycle (GGC), is on the luminal membrane. Pyroglutamate (oxoproline), an intracellular product of GGC, stimulated Na + ‐dependent transport of glutamate by 46%, whereas facilitative glutamate uptake in luminal membranes was inhibited. This relationship between GGC and glutamate transporters may be part of a regulatory mechanism that accelerates glutamate removal from brain.