期刊
BRAIN BEHAVIOR AND IMMUNITY
卷 102, 期 -, 页码 98-109出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbi.2022.02.019
关键词
IL-33; Amygdala; Anxiety; BDNF
资金
- National Natural Science Foundation of China [81971471, 82173105, 81771775]
- Shandong Provincial Key Research and Development Program (Major Scientific and Technological Innovation Project) [2019JZZY011113]
- China Postdoctoral Science Foundation [2019M662338]
- Natural Science Foundation of Shandong Province [ZR2020QC087]
Hyper-inflammatory reaction can activate anxiety circuits by suppressing BDNF and GABAergic neurons transmission.
Hyper-inflammatory reaction plays a crucial role in the pathophysiology of depression and anxiety disorders. However, the mechanisms underlying inflammation-induced anxiety changes remain poorly understood. Here, we showed that in the lipopolysaccharide (LPS)-induced anxiety model, Interleukin (IL)-33, a member of the IL-1 family, was up-regulated in the basolateral amygdala, and IL-33 deficiency prevent anxiety-like behavior. Overexpression of IL-33 in amygdalar astrocytes led to anxiety-like response via repressing brain-derived neurotrophic factor (BDNF) expression. Mechanically, IL-33 suppressed BDNF expression through NF-kappa B pathway to impair GABAergic transmission in the amygdala and NF-kappa B inhibitor abolished the effect of IL-33 on anxiety. Administration of an inverse GABAA receptor agonist increased the anxiety of IL-33-deficient mice. These results reveal that inflammatory response can activate anxiogenic circuits by suppressing BDNF and GABAergic neurons transmission, suggesting that IL-33 in basolateral amygdalar is a linker between inflammation and anxiety.
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