Glutamate uptake is decreased tardively in the spinal cord of FALS mice
作者:
Thierry Canton,
Jeremy Pratt,
Jean-Marie Stutzmann,
Assunta Imperato,
Alain Boireau,
期刊:
NeuroReport
(OVID Available online 1998)
卷期:
Volume 9,
issue 5
页码: 775-778
ISSN:0959-4965
年代: 1998
出版商: OVID
关键词: Familial amyotrophic lateral sclerosis;Glutamate;Transgenic mouse model;Transport;Uptake
数据来源: OVID
摘要:
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.
点击下载:
PDF
(289KB)
返 回