The NEGR1 (neuronal growth regulator 1) gene has been associated with schizophrenia phenotype in GWAS studies and its expression has been found to be altered in the brains of patients with schizophrenia spectrum disorders. As altered profile of circulating kynurenine pathway metabolites has been linked with schizophrenia spectrum disorders as well, we aimed to find the differences in the brain and blood serum metabolite levels between wild-type mice and Negr1-deficient mice using MK-801 (dizocilpine) and a high-fat diet. The results suggest that kynurenine metabolism is strongly biased towards kynurenic acid production in Negr1-deficient mice, while significantly less quinolinic acid is produced compared to control mice. As kynurenic acid is an NMDA receptor antagonist and quinolinic acid is the agonist, we also tried to find the main NMDA receptor subunit influenced by the changed metabolite levels. We found that Grin2b subunit seems to be the best candidate for the dysfunction of the NMDA receptor in the schizophrenia mouse models compared to the other NMDA receptor subunits. In addition, we hypothesised that a high-fat diet would have a bigger effect on the Negr1-deficient mice’s blood serum metabolite levels, but that surprisingly was not the case. Altogether this study shows that the kynurenine pathway plays an important role in the development of the schizophrenia phenotype through kynurenic acid and quinolinic acid.