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Background  The protozoan parasite  Toxoplasma gondii  infects and alters the neurotransmission in cerebral cortex and other brain regions, leading to neurobehavioral and neuropathologic changes in humans and animals. However, the molecules that contribute to these changes remain largely unknown.    Methods  We have investigated the impact of  T. gondii  infection on the overall metabolism of mouse cerebral cortex. Mass-spectrometry-based metabolomics and multivariate statistical analysis were employed to discover metabolomic signatures that discriminate between cerebral cortex of  T. gondii -infected and uninfected control mice.    Results  Our results identified 73, 67 and 276 differentially abundant metabolites, which were involved in 25, 37 and 64 pathways at 7, 14 and 21 days post-infection (dpi), respectively. Metabolites in the unsaturated fatty acid biosynthesis pathway were upregulated as the infection progressed, indicating that  T. gondii  induces the biosynthesis of unsaturated fatty acids to promote its own growth and survival. Some of the downregulated metabolites were related to pathways, such as steroid hormone biosynthesis and arachidonic acid metabolism. Nine metabolites were identified as  T. gondii  responsive metabolites, namely galactosylsphingosine, arachidonic acid, LysoSM(d18:1),  l -palmitoylcarnitine, calcitetrol, 27-Deoxy-5b-cyprinol,  l -homophenylalanine, oleic acid and ceramide (d18:1/16:0).    Conclusions  Our data provide novel insight into the dysregulation of the metabolism of the mouse cerebral cortex during  T. gondii  infection and have important implications for studies of  T. gondii  pathogenesis.    Electronic supplementary material  The online version of this article (10.1186/s13071-019-3623-4) contains supplementary material, which is available to authorized users.

Metabolomic signature of mouse cerebral cortex following Toxoplasma gondii infection