SLC1A3 and Leber hereditary optic neuropathy: Functional disturbances in EAAT-dependent glutamate uptake was previously described in cybrids harboring Leber hereditary optic neuropathy mutations, in which complex-I-deficiency-induced oxidative stress led to an EAAT1 inhibition and a lower glutamate uptake capacity, a phenomenon that was proposed to underlie neuron death [35,36].