Involvement of Inflammasome Activation in Lipopolysaccharide-induced Mice Depressive-like Behaviors
- Resource Type
- Academic Journal
- Authors
- Zhang, Yi; Liu, Lei; Peng, Yun-Li; Liu, Yun-Zi; Wu, Teng-Yun; Shen, Xiao-Liang; Zhou, Jiang-Rui; Sun, Ding-Ya; Huang, Ai-Jun; Wang, Xia; Wang, Yun-Xia; Jiang, Chun-Lei
- Source
- CNS: Neuroscience And Therapeutics. Feb 01, 2014 20(2):119-124
- Subject
- Language
- English
- ISSN
- 1755-5930
AIMS:: The NLRP3 inflammasome is a cytoplasmic multiprotein complex of the innate immune system that regulates the cleavage of interleukin-1β and interleukin-18 precursors. It can detect a wide range of danger signals and trigger a series of immune-inflammatory reactions. There were plenty of studies indicating that activation of the immune system played pivotal roles in depression. However, the underlying mechanisms of immune-depression interactions remained elusive and there was no report about the involvement of inflammasome activation in depression. METHODS:: We established an acute depression mouse model with lipopolysaccharide to explore the involvement of inflammasome activation in depression. RESULTS:: The lipopolysaccharide-treated mice displayed depressive-like behaviors and pro-inflammatory cytokine interleukin-1β protein and mRNA levels significantly increased. The NLRP3 inflammasome mRNA expression level also significantly elevated in depressed mice brain. Pretreatment with the NLRP3 inflammasome inhibitor Ac-YVAD-CMK significantly abrogated the depressive-like behaviors induced by lipopolysaccharide. CONCLUSION:: These data suggest for the first time that the NLRP3 inflammasome is involved in lipopolysaccharide-induced mice depressive-like behaviors. The NLRP3 inflammasome may be a central mediator between immune activation and depression, which raises the possibility that it may be a more specific target for the depression treatments in the near future.