ArticleInflammopharmacology2021
The role of dorsal root ganglia alpha-7 nicotinic acetylcholine receptor in complete Freund's adjuvant-induced chronic inflammatory pain.
Article in Inflammopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 17 citations in OpenAlex.
- Upregulation of AK7 in ACC-VTA glutamatergic projections contributes to chronic inflammation pain in male mice.EMBO reports · 2026Article
- Nicotinic acetylcholine receptors in pain modulation.Frontiers in pharmacology · 2026Review
- Peripheral Parasympathetic Networks in Pain: A Systems-Level Review of Mechanisms and Modulations.Cellular and molecular neurobiology · 2025Review
- MiR-31-5p regulates the neuroinflammatory response via TRAF6 in neuropathic pain.Biology direct · 2024Article
- Human-specific duplicate CHRFAM7A gene is associated with more severe osteoarthritis and amplifies pain behaviours.Annals of the rheumatic diseases · 2023Article
- Nicotinic acetylcholine receptors: Therapeutic targets for novel ligands to treat pain and inflammation.Pharmacological research · 2023Review
- Targeting α7 nicotinic acetylcholine receptors for chronic pain.Frontiers in molecular neuroscience · 2022Review
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundAlpha-7 nicotinic acetylcholine receptor (α7 nAChR) was reported to have a critical role in the regulation of pain sensitivity and neuroinflammation. However, the expression level of α7 nAChR in dorsal root ganglion (DRG) and the underlying neuroinflammatory mechanisms associated with hyperalgesia are still unknown.
methodsIn the present study, the expression and mechanism of α7 nAChR in chronic inflammatory pain was investigated using a complete Freund's adjuvant (CFA)-induced chronic inflammatory pain model. Subsequently, a series of assays including immunohistochemistry, western blotting, and quantitative real-time polymerase chain reaction (qRT-PCR) were performed.
resultsα7 nAChR was mostly colocalized with NeuN in DRG and upregulated after CFA injection. Microinjection of α7 nAChR siRNA into ipsilateral L4/5 DRGs aggravated the CFA-induced pain hypersensitivity. Intrathecal α7 nAChR agonist GTS-21 attenuated the development of CFA-induced mechanical and temperature-related pain hypersensitivities. In neuronal the SH-SY5Y cell line, the knockdown of α7 nAChRs triggered the upregulation of TRAF6 and NF-κB under CFA-induced inflammatory conditions, while agitation of α7 nAChR suppressed the TRAF6/NF-κB activation. α7 nAChR siRNA also exacerbated the secretion of pro-inflammatory mediators from LPS-induced SH-SY5Y cells. Conversely, α7 nAChR-specific agonist GTS-21 diminished the release of interleukin-1beta (IL-1β), IL-6, IL-8, and tumor necrosis factor-α (TNFα) in SH-SY5Y cells under inflammatory conditions. Mechanistically, the modulation of pain sensitivity and neuroinflammatory action of α7 nAChR may be mediated by the TRAF6/NF-κB signaling pathway.
conclusionsThe findings of this study suggest that α7 nAChR may be potentially utilized as a therapeutic target for therapeutics of chronic inflammatory pain.
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