|
|
|
|
In patients with ALS,there was a marked decrease in the maximal velocity of transport for high-affinity glutamate uptake in synaptosomes from spinal cord(-59 percent,P<0.001),motor cortex(-70 percent,P<0.001),and somatosensory cortex(-39 percent,P<0.05),but not in those from visual cortex,striatum,or hippocampus.The affinity of the transporter for glutamate was not altered.No abnormalities in glutamate transport were found in synaptosomes from patients with other chronic neurodegenerative disorders.The transport of y-aminobutyric acid and phenylalanine was normal in patients with ALS.Conclusions.ALS is associated with a defect in high-affinity glutamate transport that has disease,region,and chemical specificity.Defects in the clearance of extracellular glutamate because of a faulty transporter could lead to neurotoxic levels of extracellular glutamate and thus be pathogenic in ALS. |
|