E, Xenopus/Amphibian,citatory amino acid transporter 3 (EAAT3) transports L-glutamate and L- and D-aspartate, which is essential for terminating the postsynaptic action of glutamate by rapidly removing released glutamate from the synaptic cleft. Defects in EAAT3 have been linked to dicarbo, Xenopus/Amphibian,ylicamino aciduria, also known as glutamate-aspartate transport defect. This is a defect in renal and intestinal transport of glutamic and aspartic acid and is associated with moderate hyperprolinemia.