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

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


  • Peghini P
  • Janzen J
  • Stoffel W


The EMBO journal

Publication Data

July 1, 1997

Associated Grants


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