Abstract

Depression, characterized by low mood, is a complex mental disorder that is a serious threat to human health. Depression is thought to be caused by a combination of genetic, environmental and psychological factors. However, the pathophysiology of depression remains unclear. In the present study, we found that Dcf1 knockout (KO) mice had depression-like symptoms and disruptive changes in gamma-aminobutyric acid (GABA) concentration and GABA receptor expression were found in the hippocampus of Dcf1 KO and WT mice. Furthermore, the gut microbiota composition of Dcf1 KO mice was significantly different from that of wildtype (WT) mice and Dcf1 KO mice showed lower Firmicutes and Lactobacillus content compared to WT mice. In addition, the depression-like behavior of Dcf1 KO mice was alleviated by the administration of microbiota. More surprisingly, after treatment with Lactobacillus murine and Lactobacillus reuteri , two Lactobacillus species with proportionally greater differences in content between the WT and KO groups, KO mice showed similar GABA content, as well as restored GABA-related receptor expression, as the WT group. Our data elucidated a possible mechanism of depression induction by gut microbiota in Dcf1 KO mice and provide a new avenue to explore the treatment of depression by gut microbiota.