| First Author | Zhuang X | Year | 2022 |
| Journal | Brain Behav Immun | Volume | 102 |
| Pages | 98-109 | PubMed ID | 35181439 |
| Mgi Jnum | J:321622 | Mgi Id | MGI:6887245 |
| Doi | 10.1016/j.bbi.2022.02.019 | Citation | Zhuang X, et al. (2022) IL-33 in the basolateral amygdala integrates neuroinflammation into anxiogenic circuits via modulating BDNF expression. Brain Behav Immun 102:98-109 |
| abstractText | 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-kappaB pathway to impair GABAergic transmission in the amygdala and NF-kappaB 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. |
