ArticleJournal of neuroinflammation2023
Microglia sustain anterior cingulate cortex neuronal hyperactivity in nicotine-induced pain.
Article in Journal of neuroinflammation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Vascular integrity and immune infiltration in SCI pain: Can exercise tip the balance?Experimental neurology · 2026Article
- 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
- Functional connectivity changes in the thalamocortical network due to neck pain and the multiscale regulatory effects of acupuncture: a cross-scale multi-omics neuroimaging study.Frontiers in neuroscience · 2026Article
- Cre-driven tdTomato expression unexpectedly confers resistance to peripheral but not central lupus in dLckCre mice.Journal of translational autoimmunity · 2025Article
- Inhibition of mPFC norepinephrine improved chronic post-thoracotomy pain in adult rats.Annals of medicine · 2025Article
- Dorsoventral photobiomodulation therapy safely reduces inflammation and sensorimotor deficits in a mouse model of multiple sclerosis.Journal of neuroinflammation · 2024Article
- Santacruzamate A Alleviates Pain and Pain-Related Adverse Emotions through the Inhibition of Microglial Activation in the Anterior Cingulate Cortex.ACS pharmacology & translational science · 2024Article
- Melatonin Induces Analgesic Effects through MTResearch (Washington, D.C.) · 2024Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLong-term smoking is a risk factor for chronic pain, and chronic nicotine exposure induces pain-like effects in rodents. The anterior cingulate cortex (ACC) has been demonstrated to be associated with pain and substance abuse. This study aims to investigate whether ACC microglia are altered in response to chronic nicotine exposure and their interaction with ACC neurons and subsequent nicotine-induced allodynia in mice.
methodsWe utilized a mouse model that was fed nicotine water for 28 days. Brain slices of the ACC were collected for morphological analysis to evaluate the impacts of chronic nicotine on microglia. In vivo calcium imaging and whole-cell patch clamp were used to record the excitability of ACC glutamatergic neurons.
resultsCompared to the vehicle control, the branch endpoints and the length of ACC microglial processes decreased in nicotine-treated mice, coinciding with the hyperactivity of glutamatergic neurons in the ACC. Inhibition of ACC glutamatergic neurons alleviated nicotine-induced allodynia and reduced microglial activation. On the other hand, reactive microglia sustain ACC neuronal excitability in response to chronic nicotine, and pharmacological inhibition of microglia by minocycline or liposome-clodronate reduces nicotine-induced allodynia. The neuron-microglia interaction in chronic nicotine-induced allodynia is mediated by increased expression of neuronal CX3CL1, which activates microglia by acting on CX3CR1 receptors on microglial cells.
conclusionTogether, these findings underlie a critical role of ACC microglia in the maintenance of ACC neuronal hyperactivity and resulting nociceptive hypersensitivity in chronic nicotine-treated mice.
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