SLC1A7 (EAAT5) is a high-affinity glutamate transporter that mediates sodium-dependent uptake of L-glutamate, L-aspartate, and D-aspartate 1. The transporter functions as a symporter, coupling the uptake of one amino acid molecule with two to three Na⁺ ions and one H⁺ ion, while counter-transporting one K⁺ ion 2. This coupling mechanism enables uphill transport against concentration gradients, protecting cells from glutamate excitotoxicity 2. In the retina, SLC1A7 acts primarily as an inhibitory presynaptic receptor at rod bipolar cell terminals, functioning as a glutamate-gated chloride channel that regulates visual processing [UniProt]. Beyond neurotransmission, SLC1A7 participates in amino acid metabolism across tissues, playing roles in metabolic homeostasis and nutrient utilization 3. Recent evidence suggests SLC1A7 influences neurodevelopment, as its expression is altered by milk oligosaccharides affecting hippocampal gene expression and cognitive development 4. Dysregulation of SLC1A7 has been associated with disease pathogenesis; variants were identified in familial Graves' disease 5, and altered expression correlates with aggressive cancer phenotypes and poor prognosis in gastric cancer 3. These findings establish SLC1A7 as a multifunctional transporter with implications for neurological function, metabolism, and disease susceptibility.