Article
- The EMBO Journal (1997) 16, 3822 - 3832
- doi:10.1093/emboj/16.13.3822
Glutamate transporter EAAC-1-deficient mice develop dicarboxylic aminoaciduria and behavioral abnormalities but no neurodegeneration
Pietro Peghini1, Julia Janzen1 and Wilhelm Stoffel1
-
Laboratory of Molecular Neuroscience, Institute of Biochemistry, Faculty of Medicine, University of Cologne, Joseph-Stelzmann-Stra
e 52, D-50931 Cologne, Germany
Correspondence to:
Pietro Peghini,
Received 2 January 1997; Revised 26 March 1997
Abstract
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.
Keywords:
- behavioral abnormalities,
- deficient mice,
- dicarboxylic aminoaciduria,
- EAAC-1,
- glutamate neurotransmitter transporters
