| Literature DB >> 26554725 |
Motamed Elsayed Mahmoud1, Fumiaki Ihara2, Ragab M Fereig2, Maki Nishimura2, Yoshifumi Nishikawa3.
Abstract
Although Toxoplasma gondii (T. gondii) infection is relevant to many psychiatric disorders, the fundamental mechanisms of its neurobiological correlation with depression are poorly understood. Here, we show that reactivation of chronic infection by an immunosuppressive regimen caused induction of depressive-like behaviors without obvious sickness symptoms. However, the depression-related behaviors in T. gondii-infected mice, specifically, reduced sucrose preference and increased immobility in the forced-swim test were observed at the reactivation stage, but not in the chronic infection. Interestingly, reactivation of T. gondii was associated with production of interferon-gamma and activation of brain indoleamine 2, 3-dioxygenase, which converts tryptophan to kynurenine and makes it unavailable for serotonin synthesis. Furthermore, serotonin turnover to its major metabolite, 5-hydroxyindoleacetic acid, was also enhanced at the reactivation stage. Thus, enhanced tryptophan catabolic shunt and serotonin turnover may be implicated in development of depressive-like behaviors in mice with reactivated T. gondii.Entities:
Keywords: 3 dioxygenase; Depressive-like behaviors; Indoleamine 2; Mouse; Reactivation; Toxoplasma gondii
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Year: 2015 PMID: 26554725 DOI: 10.1016/j.bbr.2015.11.005
Source DB: PubMed Journal: Behav Brain Res ISSN: 0166-4328 Impact factor: 3.332