Abstract
EAAC-1 played key functions in the regulation of synaptic L-glutamate concentration during neurotransmission, and may prevent glutamate neurotoxicity. It has a unique distribution pattern in the central nervous system (CNS), and neuronal EAAC-1 is expressedin small intestine and kidney. EAAC-1–/– mice develop dicarboxylic aminoaciduria. While no neurodegenerative changes are seen in over 12 months of observation. The phenotype of the EAAC-1 mutants exhibited a significant reduction in spontaneous locomotor activity.
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