The transport of Glu into the cells by the EAAT transporters is coupled to the Na⁺ and K⁺ electrochemical gradient as a driving force. Hence, the uptake of Glu is dependent on the co-transport of three Na⁺ and one H⁺ ions, and the counter transport of one K⁺ ion.  

In addition, to the well documented Glu uptake, the EAAT transporters show a Glu-independent Cl^- conductance. The physiological significance of the Cl^- current through the EAATs is currently unknown.^1,2

EAAT1 as well as EAAT2, is expressed predominantly in glia cells (hence its original name: glial glutamate transporter or GLAST), while EAAT3, EAAT4 and EAAT5 are mostly expressed in neurons.

Three vesicular glutamate transporters (VGLUTs) have been cloned: BNPI/VGLUT1 (a brain-specific sodium dependent inorganic phosphate (Pi) transporter), and its homologs DNPI/VGLUT2 (differentiation-associated sodium-dependent Pi transporter) and VGLUT3³. These transporters mediate glutamate uptake inside presynaptic vesicles and are anatomical and functional markers of glutamatergic excitatory transmission⁴.