| First Author | Peghini P | Year | 1997 |
| Journal | EMBO J | Volume | 16 |
| Issue | 13 | Pages | 3822-32 |
| PubMed ID | 9233792 | Mgi Jnum | J:41613 |
| Mgi Id | MGI:894143 | Doi | 10.1093/emboj/16.13.3822 |
| Citation | Peghini P, et al. (1997) Glutamate transporter EAAC-1-deficient mice develop dicarboxylic aminoaciduria and behavioral abnormalities but no neurodegeneration. EMBO J 16(13):3822-32 |
| abstractText | 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. |
