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Published in: Journal of Neural Transmission 8/2014

01-08-2014 | Translational Neurosciences - Review article

Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression?

Authors: Robert Dantzer, Adam K. Walker

Published in: Journal of Neural Transmission | Issue 8/2014

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Abstract

Chronic inflammation in physically ill patients is often associated with the development of symptoms of depression. The mechanisms that are responsible for inflammation-associated depression have been elucidated over the last few years. Kynurenine produced from tryptophan in a reaction catabolized by indoleamine 2,3 dioxygenase is transported into the brain where it is metabolized by microglial enzymes into a number of neurotropic compounds including quinolinic acid, an agonist of N-methyl-d-aspartate receptors. Quinolinic acid can synergize with glutamate released by activated microglia. This chain of events opens the possibility to treat inflammation-induced depression using therapies that target the transport of kynurenine through the blood–brain barrier, the production of quinolinic acid and glutamate by activated microglia, or the efflux of glutamate from the brain to the blood.
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Metadata
Title
Is there a role for glutamate-mediated excitotoxicity in inflammation-induced depression?
Authors
Robert Dantzer
Adam K. Walker
Publication date
01-08-2014
Publisher
Springer Vienna
Published in
Journal of Neural Transmission / Issue 8/2014
Print ISSN: 0300-9564
Electronic ISSN: 1435-1463
DOI
https://doi.org/10.1007/s00702-014-1187-1

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