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Glutamate transporter EAAC-1-deficient mice develop dicarboxylic aminoaciduria and behavioral abnormalities but no neurodegeneration.

The EMBO journal | Jul 1, 1997

http://www.ncbi.nlm.nih.gov/pubmed/9233792

Four L-glutamate neurotransmitter transporters, the three Na(+)-dependent GLAST-1, GLT-1 and EAAC-1, and the Cl(-)-dependent EAAT-4, form a new family of structurally related integral plasma membrane proteins with different distribution in the central nervous system. They may have pivotal functions in the regulation of synaptic L-glutamate concentration during neurotransmission and are believed to prevent glutamate neurotoxicity. To investigate the specific physiological and pathophysiological role of the neuronal EAAC-1, which is also expressed in kidney and small intestine, we have generated two independent mouse lines lacking EAAC-1. eaac-1(-/-) mice develop dicarboxylic aminoaciduria. No neurodegeneration has been observed during a period of >12 months, but homozygous mutants display a significantly reduced spontaneous locomotor activity.

Pubmed ID: 9233792 RIS Download

Mesh terms: Amino Acid Sequence | Amino Acid Transport System X-AG | Amino Acids, Dicarboxylic | Animals | Brain | Carrier Proteins | Epilepsy | Excitatory Amino Acid Transporter 1 | Female | Gene Targeting | Glutamate Plasma Membrane Transport Proteins | Glutamic Acid | Mice | Mice, Inbred BALB C | Molecular Sequence Data | Motor Activity | Pentylenetetrazole | Phenotype | Rats | Symporters

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