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J Neural Transm (Vienna). 2014 Aug;121(8):925-32. doi: 10.1007/s00702-014-1187-1. Epub 2014 Mar 15.

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

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Division of Internal Medicine, Department of Symptom Research, MD Anderson Cancer Center, 1400 Pressler Street, Houston, TX, 77030, USA,


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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