The termination of chemical neurotransmission in the CNS involves the rapid
removal of neurotransmitter from synapses by specific transport systems. S
uch mechanism operates for the three major amino acid neurotransmitters glu
tamate, gamma -aminobutyric acid (GABA) and glycine. To date, five differen
t high-affinity Naf-dependent glutamate (Glu) transporters have been cloned
: GLT1, GLAST, EAAC1, EAAT4 and EAAT5. The first two are expressed mainly b
y glial cells, and seem to be the predominant Glu transporters in the brain
. A major function of Glu uptake in the nervous system is to prevent extrac
ellular Glu concentrations from raising to neurotoxic levels in which glial
transporters seem to play a critical role in protecting neurons from gluta
mate-induced excitotoxicity. Under particular conditions, glial GluTs have
been shown to release Glu by reversal of activity, in a Ca2+- and energy-in
dependent fashion. Furthermore, an activity of these transporters as ion ch
annels or transducing units coupled to G-proteins has recently been reporte
d. The localization, stoichiometry, and regulation of glial GluTs are outli
ned, as well as their possible contributions to nervous system diseases as
ALS, AD and ischemic damage. J. Neurosci. Res. 63. 453-460, 2001. (C) 2001
Wiley-Liss, Inc.