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Human excitatory amino acid transporters (EAATs) are members of a family of high affinity sodium-dependent transporter molecules that regulate neurotransmitter concentrations at the excitatory glutamatergic synapses of the mammalian central nervous system. It is believed that these proteins reduce extracellular glutamate concentration, thereby modulating synaptic signaling. In addition, EAATs may also be important for the prevention of glutamate excitotoxicity. EAAT1 is prominently expressed in the frontal cortex, hippocampus and basal ganglia and is also reported to be found in heart, placenta, lung and striated muscle. EAAT1 shares some pharmacological similarities with EAAT3 and both are potent antagonists that appear to specifically block transport mediated by EAAT2. EAAT1 transports L-glutamate and also L- and D-aspartate, acting as a symport by co-transporting sodium. EAAT1 is essential for terminating the postsynaptic action of glutamate, by rapidly removing released glutamate from the synaptic cleft.