ArticleTranslational neuroscience2020
IRF8 is crucial for the nicotine withdrawal-induced hyperalgesia in mice.
Article in Translational neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 1 citations in OpenAlex.
- Altered Regional Brain Activity Underlying the Higher Postoperative Analgesic Requirements in Abstinent Smokers: A Prospective Cohort Study.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Elevated TNF-α Leads to Neural Circuit Instability in the Absence of Interferon Regulatory Factor 8.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInterferon regulatory factor 8 (IRF8) is involved in the pathogenesis of neuropathic pain. However, whether and how IRF8 can regulate the nicotine withdrawal (NTW)-induced hyperalgesia has not been clarified.
methodsC57BL/6 mice were randomized and injected subcutaneously with saline (Control) or nicotine (3 mg/kg) three times per day for 7 consecutive days, followed by injection with mecamylamine to induce NTW. Their paw withdrawal latencies (PWLs) were measured, and the relative levels of IRF8 expression in the spinal cord tissues were determined longitudinally by western blot. The numbers of IRF8+ cells in the spinal cord tissues were examined. In addition, the NTW mice were randomized and infused intrathecally with vehicle saline (NS), control lentivirus or lentivirus for the expression of IRF8-specific shRNA for three days. Their PWLs, microglia activation, IRF8 and P2X4R and BDNF expression in the spinal cord tissues were determined.
resultsIn comparison with the Control mice, the NTW significantly decreased the PWLs but increased the relative levels of IRF8 expression and the numbers of IRF8+ cells in the spinal cord tissues of mice. IRF8-silencing significantly mitigated the NTW-decreased PWLs and attenuated the NTW-enhanced microglia activation and P2X4R and BDNF expression in the spinal cord tissues of mice.
conclusionsSpinal IRF8 is crucial for the NTW-induced hyperalgesia by enhancing microglia activation and spinal P2X4R and BDNF expression in mice. The IRF8/P2X4R/BDNF axis may be potential therapeutic targets for postoperative pain of smokers.
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