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Published on: December 22, 2008
Argon improves microglia-mediated hippocampal neuronal hyperexcitability to alleviate anxiety-like behaviors in mice
Jie Cheng1, Baiyang Zheng1, Shusu Luo1
1Institute of Special Environmental Medicine, Nantong University, Nantong 226000, China.
Abstract:
The role of inflammation in psychiatric disorders, such as anxiety, has gained increasing attention, with the hippocampus being identified as a key region involved in emotional regulation. Argon has been reported to alleviate the symptoms of psychiatric disorders; however, its underlying mechanism remains unclear. In this study, we found that argon significantly suppressed lipopolysaccharide-induced anxiety-like behaviors and attenuated hippocampal neuronal hyperexcitability in mice. By analyzing neuronal excitability following microglial depletion and subsequent repopulation, as well as assessing microglial morphology, we confirmed that microglia are key targets of inflammation and validated the inhibitory effects of argon. Electrophysiological studies and transcriptome sequencing revealed that argon inhibited the microglia-released inflammatory cytokines via the Toll-like receptor 4/nuclear factor-κB signaling pathway, thereby improving the excitability of hippocampal neurons. Collectively, this study provides evidence that the regulation of microglia may be the underlying mechanism by which argon ameliorates neuroinflammation-induced anxiety-like behaviors.
Insights
Argon significantly reduces anxiety-like behaviors and hippocampal neuronal hyperexcitability in mice by targeting microglia. This study reveals argon inhibits inflammatory cytokines via the Toll-like receptor 4/nuclear factor-κB pathway, offering a potential treatment for neuroinflammation-induced anxiety.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Inflammation is increasingly implicated in psychiatric disorders like anxiety.
- The hippocampus plays a crucial role in emotional regulation.
- The therapeutic mechanism of argon in psychiatric disorders is not well understood.
Purpose of the Study:
- To investigate the effects of argon on anxiety-like behaviors and hippocampal function.
- To elucidate the underlying mechanism of argon's action, focusing on microglia and inflammation.
Main Methods:
- Assessed anxiety-like behaviors and hippocampal neuronal excitability in mice.
- Utilized microglial depletion and repopulation models.
- Performed electrophysiological studies and transcriptome sequencing.
- Analyzed the Toll-like receptor 4/nuclear factor-κB signaling pathway.
Main Results:
- Argon suppressed lipopolysaccharide (LPS)-induced anxiety-like behaviors and hippocampal neuronal hyperexcitability.
- Microglia were confirmed as key targets of inflammation, with argon demonstrating inhibitory effects.
- Argon inhibited microglia-released inflammatory cytokines via the TLR4/NF-κB pathway.
Conclusions:
- Argon ameliorates neuroinflammation-induced anxiety-like behaviors.
- The regulation of microglia and their inflammatory cytokine release is the likely mechanism of argon's therapeutic effect.
- This study highlights microglia as a potential therapeutic target for anxiety disorders.
