Considering the genotypic and biological diversity of T. cruzi strains ( Zingales et al., 2012), we wondered whether the depressive

profile induced by infection with the type I Colombian strain could also be elicited by the distinct type II Y strain. To investigate this question, C3H/He mice were infected with 500-bt of the Y strain and followed daily for parasitemia and mortality. Parasitemia was detected as early as 4 dpi, peaked at 7–8 dpi and was controlled subsequently. No circulating parasite was detected at or after 18 dpi, which CP-868596 solubility dmso marked the resolution of acute infection and the onset of chronic infection ( Fig. 4A). All the infected animals survived (data not shown). Next, we investigated whether the mice appeared to be depressed with the TST. A significant increase in immobility was detected at 7 dpi (p < 0.05; at the peak of parasitemia) and reached a maximum at 14 dpi (p < 0.001). At 28 and 35 dpi, the immobility of infected mice was similar (p > 0.05) to that of sex- and age-matched NI controls ( Fig. 4B). Importantly, the duration of immobility time did not correlate with CNS parasitism: at 7 dpi in the Y strain, when behavioral alterations were first detected, no parasites

were found by IHS in brain sections. A few parasites were detected in the CNS tissue at 14 dpi. CNS parasitism peaked at 28 dpi and declined at 35 dpi ( Fig. 4C and D). CNS parasitism was found mainly in the cerebellum (data not shown) and hippocampus ( Fig. 4D) at 35 dpi when depressive-like SSR128129E behavior was not detected in the Y-strain-infected C3H/He mice ( Fig. 4B). Thus, there was no association between CNS parasitism and depressive-like selleck inhibitor behavior. Furthermore, the type I Colombian T. cruzi strain, but not the type II Y strain, induced chronic depressive-like

behavior in mice. Depressive-like behavior was detected in the Colombian-infected C3H/He mice at 30 dpi and persisted until 90 dpi (Fig. 3A and B). Although a consistent, slight increase in immobility time was detected at 14 dpi, the onset of depressive-like behavior in the Colombian-infected C3H/He mice occurred at 21 dpi, when a significant increase in immobility was detected, and persisted during the chronic phase (Fig. 5A; p < 0.05; H (5) = 29.46). Given the participation of tryptophan-degrading enzymes such as IDO in depression ( Dantzer et al., 2008), we investigated the status of IDO mRNA in the CNS of T. cruzi-infected mice. Compared with NI controls, an increase in IDO mRNA expression was observed in the CNS of T. cruzi-infected mice during the acute (30 dpi) and chronic (90 dpi) phases of infection ( Fig. 5B). To further investigate depressive-like behavior during T. cruzi infection, Colombian-infected C3H/He and C57BL/6 mice were subjected to treatment with the selective serotonin reuptake inhibitor (SSRI) antidepressant fluoxetine (FX) from 14 to 34 dpi and analyzed at 35 dpi ( Fig. 5C). As expected ( D’Souza et al., 2004), FX-treated mice presented body weight loss (p < 0.001; H (3) = 19.