Clinical Psychopharmacology and Neuroscience indexed in CAS, DOI/Crossref, EMBASE, Korea Citation Index (KCI), KoreaMed, Korea Medical Citation Index (KoMCI), PubMed, PubMed Central (PMC), SCOPUS, SCI-expanded (SCIE), and Google Scholar:eISSN 2093-4327   pISSN 1738-1088

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Fig. 2. Kynurenine pathway abnormalities in depression and schizophrenia. An illustration of main biochemical abnormalities in two major psychiatric disorders, i.e., depression and schizophrenia. In the brain, proinflammatory cytokines and other inflammatory mediators cause induction of indoleamine 2,3-dioxygenase and triggering of microglia with increased production of quinolinic acid which is an agonist at the N-methyl-D-aspartate receptor and also acts as an excitotoxin. This mechanism is thought to underlie the expression of the depressive phenotype during inflammatory processes. On the contrary in schizophrenia, kynurenine amino transferase, another key kynurenine pathway enzyme is expressed which increases the formation of kynurenic acid. The latter is the only known endogenous NMDAR antagonist and acting through intermediary mechanisms, indirectly increases dopaminergic neurotransmission in the mesolimbic pathway, which is the chief abnormality in schizophrenia. See also text for a full description of KP abnormalities in neuropsychiatric disorders. NMDAR, NMDA receptor; KP, kynurenine pathway; IDO, indoleamine 2,3-dioxygenase; KAT, kynurenine aminotransferase; KMO, kynurenine 3-monooxygenase.
Clinical Psychopharmacology and Neuroscience 2020;18:507~526
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