Glutamate uptake is decreased tardively in the spinal cord of FALS mice
Glutamate uptake is decreased tardively in the spinal cord of FALS mice
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DOI：
10.1097/00001756-199803300-00001
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发表时间：
1998-03-30
期刊：
影响因子：
1.7
通讯作者：
Boireau, A
中科院分区：
文献类型：
--
作者：
Canton, T;Pratt, J;Boireau, A
本研究检测了表达人类铜/锌超氧化物歧化酶（SOD1）显性突变的小鼠脊髓突触体制剂中谷氨酸的高亲和力Na+依赖性摄取，并代表了肌萎缩性侧索硬化症（ALS）的动物模型。在他们的一生中，他们的肌肉力量也通过握力牵引测试进行监测。高亲和力Na+依赖性[H-3]谷氨酸摄取在120 ~ 150日龄之间下降。150 d时，整个脊髓突触体的V-max显著下降（-40.2%,p < 0.001）， K-m无变化。这一显著下降发生在动物死亡前一周（157.2 +/- 2.2天），对应于肌肉力量的显著下降（120至140天之间损失25%，p < 0.001）。因此，FALS小鼠模型再现了在散发性或家族性ALS患者中报道的谷氨酸摄取减少。这些结果讨论了可能迟发性参与谷氨酸摄取缺乏在人类ALS。(C) 1998快速科学有限公司
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 [H-3]glutamate was decreased between 120 and 150 days of age. A marked and significant decrease in V-max (-40.2%; p < 0.001) on whole spinal cord synaptosomes was observed at 150 days, with no change in K-m. 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. (C) 1998 Rapid Science Ltd.