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The complement-derived anaphylatoxin C5a increases microglial GLT-1 expression and glutamate uptake in a TNF-alpha-independent manner.

Journal article
Authors Mikael Persson
Marcela Pekna
Elisabeth Hansson
Lars Rönnbäck
Published in The European journal of neuroscience
Volume 29
Issue 2
Pages 267-74
ISSN 1460-9568
Publication year 2009
Published at Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Pages 267-74
Language en
Keywords Animals, Animals, Newborn, Biological Transport, Active, drug effects, physiology, Cells, Cultured, Complement C5a, pharmacology, Cytoprotection, drug effects, physiology, Dose-Response Relationship, Drug, Encephalitis, chemically induced, metabolism, physiopathology, Excitatory Amino Acid Transporter 2, drug effects, metabolism, Extracellular Fluid, drug effects, metabolism, Gliosis, chemically induced, metabolism, physiopathology, Glutamic Acid, metabolism, Lipopolysaccharides, pharmacology, Microglia, drug effects, metabolism, Rats, Rats, Sprague-Dawley, Tumor Necrosis Factor-alpha, metabolism, Up-Regulation, drug effects, physiology
Subject categories Neuroscience


Microglia can express Na+-dependent high-affinity glutamate transporters during pathological conditions in the CNS. The transporter expression seems to be activation dependent, and we therefore sought to identify factors that could induce it, in addition to the well-known effect of lipopolysaccharide (LPS) that is mediated by tumour necrosis factor-alpha (TNF-alpha). The complement-derived anaphylatoxins C3a and C5a are of potential interest as the complement system is activated in nearly all insults to the nervous system, and both C3a and C5a have been shown to protect against excitotoxicity. We have found that C5a, but not C3a, increased the expression of the microglial glutamate transporter GLT-1 in a dose-dependent manner without eliciting or modulating the release of TNF-alpha. However, the increase was not as prominent as the one induced by LPS, indicating that the microglia are in different activity states. The increase in microglial GLT-1 expression led to an increased functional uptake of glutamate without affecting the release. This suggests that C5a-stimulated microglia can be self- and neuroprotective by removing extracellular glutamate.

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