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. Author manuscript; available in PMC: 2020 Jan 1.
Published in final edited form as: Trends Neurosci. 2018 Oct 13;42(1):23–42. doi: 10.1016/j.tins.2018.09.008

Figure 3. Inflammation-induced excitotoxicity through the kynurenine pathway.

Figure 3.

(A) Pro-inflammatory cytokines stimulate indoleamine 2,3-dioxygenase (IDO) in peripheral macrophages, resulting in production of kynurenine that crosses the blood-brain barrier. (B) Microglia convert kynurenine to quinolinic acid (QUIN). (C) In turn, QUIN exerts possibly neurotoxic effects, in part by (D) activating N-methyl-d-aspartate (NMDA) receptors, and (E) by decreasing glutamate reuptake, which increases glutamate release to potentially excitotoxic levels [106]. DA, dopamine; IDO, indoleamine 2,3-dioxygenase; NMDA, N-methyl-d-aspartate.