| Literature DB >> 28641538 |
Yu-Yan Hu1, Li Li2, Xiao-Hui Xian1, Min Zhang1, Xiao-Cai Sun1, Shu-Qin Li1, Xin Cui1, Jie Qi1, Wen-Bin Li1.
Abstract
Glutamate is the primary excitatory neurotransmitter in the mammalian central nervous system, which plays an important role in many aspects of normal brain function such as neural development, motor functions, learning and memory etc. However, excessive accumulation of glutamate in the extracellular fluid will induce excitotoxicity which is considered to be a major mechanism of cell death in brain ischemia. There is no enzyme to decompose the glutamate in extracellular fluid, so extracellular glutamate homeostasis within the central nervous system is mainly regulated by the uptake activity of excitatory amino acid transporters. Among the five excitatory amino acid transporters, glial glutamate transporter-1 (GLT-1) is responsible for 90% of total glutamate uptake. Thus, GLT-1 is essential for maintaining the appropriate level of extracellular glutamate, and then limiting excitotoxicity of glutamate in central nervous system. Therefore, the regulation of GLT-1 might be a potential therapeutic target for ischemic brain injury. This review summarizes recent advances including our findings in the methods or medicine that could protect neurons against brain ischemic injury via upregulation of GLT-1 and discuss the possible application of these strategies. Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.org.Entities:
Keywords: GLT-1; Glutamate transporters; brain ischemia; cAMP; dexamethasone; estrogen; histamine; preconditioning; β-lactamszzm321990antibiotics
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Year: 2017 PMID: 28641538 DOI: 10.2174/1381612823666170622103852
Source DB: PubMed Journal: Curr Pharm Des ISSN: 1381-6128 Impact factor: 3.116