ArticleMolecular medicine (Cambridge, Mass.)2025
GluR2 overexpression in ACC glutamatergic neurons alleviates cancer-induced bone pain in rats.
Article in Molecular medicine (Cambridge, Mass.), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed.
- CRH neurons in the AM-ACC circuit drive chronic pain and anxiety comorbidity.Frontiers in neuroscience · 2026Article
- Energy Metabolism and Cancer Pain: A Pathway to Innovative Treatment Strategies.Current topics in medicinal chemistry · 2026Review
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Abstract
backgroundCancer-induced bone pain (CIBP) is a complex chronic pain with poorly understood mechanisms. The anterior cingulate cortex (ACC) plays a critical role in processing and modulating chronic pain. This study investigates how the GluR2 receptors (calcium impermeable AMPA receptors) in ACC glutamatergic neurons regulate CIBP.
methodsThe CIBP models were established by injecting Walker 256 cells into the tibia of SD rats. Paw withdrawal threshold (PWT) and paw withdrawal latency (PWL) were used as indicators of hyperalgesia. The immunofluorescence staining was employed to detect the expression of c-Fos in ACC and identify the subtypes of co-labeled c-Fos
resultsThere were significant reductions in PWT and PWL of CIBP rats after Walker 256 cell injection. The ACC of CIBP rats showed increased c-Fos expression compared to sham rats, with mainly activated c-Fos co-localized with glutamatergic neurons. Optogenetic or chemogenetic activation of ACC glutamatergic neurons led to increased hyperalgesia in sham rats, while suppression of their activity alleviated hyperalgesia in CIBP rats. Calcium activity in ACC glutamatergic neurons of CIBP rats was increased with suprathreshold stimulation of von Frey filament. Notably, surface GluR2 protein and mRNA were reduced in ACC of CIBP rats. Furthermore, overexpression of GluR2 by AAV-CaMKII-GluR2 injection was decreased c-Fos expression in ACC and alleviated hyperalgesia in CIBP rats.
conclusionsThese findings suggest that decreased surface GluR2 receptors in ACC glutamatergic neurons contribute to calcium activity and excessive excitability, thereby inducing CIBP in rats. Conversely, GluR2 overexpression in ACC glutamatergic neurons alleviates CIBP in rats. This study provides a new potential therapeutic approach for targeting the GluR2 receptor to alleviate CIBP for cancer patients.
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