Laquinimod ameliorates excitotoxic damage by regulating glutamate re-uptake
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چکیده
منابع مشابه
Excitotoxic oligodendrocyte death and axonal damage induced by glutamate transporter inhibition.
Glutamate uptake is crucial to terminate glutamate signaling and to prevent excitotoxicity. The present study describes the expression of functional glutamate transporters GLAST and GLT-1 in oligodendrocytes by means of electrophysiology, uptake assays, and immunocytochemistry. Inhibition of glutamate uptake, both in oligodendrocyte cultures and in isolated optic nerves, increases glutamate lev...
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Increased levels of glutamate causing excitotoxic damage accompany many neurological disorders. A well-characterized model of excitotoxic damage involves administration of kainic acid (KA), which causes limbic seizure activity and subsequent neuronal death, particularly in the CA1 and CA3 areas of the hippocampus. Inhibition of the enzyme glycogen synthase kinase-3 (GSK-3) and cAMP levels might...
متن کاملExcitotoxic damage to white matter.
Glutamate kills neurons by excitotoxicity, which is caused by sustained activation of glutamate receptors. In recent years, it has been shown that glutamate can also be toxic to white matter oligodendrocytes and to myelin by this mechanism. In particular, glutamate receptor-mediated injury to these cells can be triggered by activation of alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid,...
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Objective(s): The present study was designed to evaluate of Metformin/Irinotecan-loaded poly-lactic-co-glycolic acid (PLGA) nanoparticles (NPs) effects on glutamate re-uptake time and receptor expression status in both glioblastoma multiforme (GBM) and cortex neuron cultures. The study was performed on glioblastoma cell line and primer cortex neuron.Materials and Methods: The re-uptake time and...
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ژورنال
عنوان ژورنال: Journal of Neuroinflammation
سال: 2018
ISSN: 1742-2094
DOI: 10.1186/s12974-017-1048-6