Anti-Depressive-like Behaviors of APN KO Mice Involve Trkb/BDNF Signaling Related Neuroinflammatory Changes
Abstract
Major depression disorder is a severe mental illness often linked with metabolic disorders. Adiponectin is an adipocyte-secreted circulatory hormone with antidiabetic and glucose/lipid modulation capacities. Studies have demonstrated the pathophysiological roles of adiponectin involved in various neurological disorders, including depression. However, the underlying mechanisms are poorly understood. Here we showed that adiponectin deprivation enhanced antidepressive-like behaviors in the LPS-induced model of depression. APN KO mice displayed increased cytokines (both pro and anti-inflammatory), accompanied by an impaired expression of adiponectin receptors (mRNA/protein level) and decreasing IBA-1 level in the cortex and primary microglia of LPS treated APN KO mice. Further, LPS-treatment significantly reduced p-NFκB expression in the microglia of APN KO mice. However, the Bay11-7082 treatment recovered p-NFκB expression in the cortex of APN KO mice in the presence of LPS. Interestingly, the antidepressant potentials of APN KO mice were abolished by TrkB antagonist K252a, IKK inhibitor Bay11-7082, and AdipoRon suggesting crosstalk between TrkB/BDNF signaling and NFκB in depression. Furthermore, the effects of Bay11-7082 were abolished by a TrkB/BDNF activator (7,8-DHF), indicating a critical role of TrkB/BDNF signaling. Taken together, these findings showed that dysregulated neuroinflammatory status and BDNF signaling might underlie the antidepressive-like behaviors of APN KO mice. NFκB elicited BDNF changes may be accountable for the pathogenesis of LPS induced depression, where APN might present an alternative therapeutic target for depressive disorders.
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BDNF may modulate the neuroinflammatory response through the m-BDNF-TrkB pathway, in addition to maintaining neuronal survival.
“BDNF may modulate the neuroinflammatory response through the m-BDNF-tropomyosin receptor kinase B (TrkB) pathway, in addition to its role in maintaining neuronal survival [33,34,35].”
From Neuroprotective Effects of Bifidobacterium breve CCFM1067 in MPTP-Induced Mouse Models of Parkinson’s Disease (2022) · cites this paper as [34]
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- Authors
- Li, W., Ali, T., Zheng, C., He, K., Liu, Z., Shah, F. A., Li, N., Yu, Z.-J., & Li, S.
- Affiliations
- Peking University (CN)
- Riphah International University (PK)
- The Seventh Affiliated Hospital of Sun Yat-sen University (CN)
- Centre for Addiction and Mental Health (CA)
- Corresponding author
- Li, Shupeng
- Venue
- Molecular Psychiatry
- Published
- 2021-10-12
- Volume
- 27
- Issue
- 2
- Pages
- 1047-1058
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- OpenAlex
- W3207349677
- Cited by
- 80
- References
- 78
- Citations by year
- 2026: 11 · 2025: 25 · 2024: 16 · 2023: 23 · 2022: 5
- FWCI
- 3.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- adiponectin, adiponectin receptors, depression, neuroinflammation, microglia, NF-κB, lipopolysaccharide-induced depression, BAY 11-7082, K252a, AdipoRon, cytokines, Iba1, major depressive disorder
- MeSH terms
- Animals, Antidepressive Agents, Lipopolysaccharides, Mice, Inbred C57BL, Signal Transduction, Brain-Derived Neurotrophic Factor, Mice, Adiponectin
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