Motor SystemsGlutamate uptake is decreased tardively in the spinal cord of FALS miceCanton, Thierry1,2; Pratt, Jeremy1; Stutzmann, Jean-Marie1; Imperato, Assunta1; Boireau, Alain1Author Information 1Rhône-Poulenc Rorer S.A., Centre de Recherche de Vitry-Alfortville, Service de neurophysiologie, 13, quai Jules Guesde BP 14, 94403 Vitry-sur-Seine Cedex, France 2Corresponding Author: Thierry Canton Received 13 November 1997; accepted 11 January 1998 NeuroReport: March 30th, 1998 - Volume 9 - Issue 5 - p 775-778 Buy Abstract 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. © Lippincott-Raven Publishers.