| First Author | Canton T | Year | 1998 |
| Journal | Neuroreport | Volume | 9 |
| Issue | 5 | Pages | 775-8 |
| PubMed ID | 9579663 | Mgi Jnum | J:103582 |
| Mgi Id | MGI:3610436 | Doi | 10.1097/00001756-199803300-00001 |
| Citation | Canton T, et al. (1998) Glutamate uptake is decreased tardively in the spinal cord of FALS mice. Neuroreport 9(5):775-8 |
| abstractText | This study examined high affinity Na+-dependent uptake of glutamate in synaptosomal preparations from spinal cord in mice that express a dominant mutation of human copper/zinc superoxide dismutase (SOD1) and represent an animal model of amyotrophic lateral sclerosis (ALS). Their muscle strength was also monitored by a grip traction test throughout their lifespan. The high affinity Na+-dependent uptake of [3H]glutamate was decreased between 120 and 150 days of age. A marked and significant decrease in Vmax (-40.2%; p < 0.001) on whole spinal cord synaptosomes was observed at 150 days, with no change in Km. This significant decrease was reached a week before the animals died (157.2 +/- 2.2 days) and corresponded to a considerable fall in muscle strength (25% loss between 120 and 140 days, p < 0.001). The FALS mouse model therefore reproduces the decrease in glutamate uptake reported in humans suffering from sporadic or familial ALS. These results are discussed in terms of a possible tardive involvement of glutamate uptake deficiency in human ALS. |
