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March 3, 2026Experimental & Molecular MedicineOpen Access

Microglial CR3-mediated synaptic pruning in the dmPFC promotes the generation and maintenance of chronic muscle pain via glutamatergic dysfunction

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Authors

MLMeiling LuoLWLikai WangYLYanan Liang

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Overview

Identifies glutamatergic dysfunction as a mechanism contributing to chronic muscle pain, suggesting new therapeutic targets.

Key Points

  • The research aims to understand how microglial CR3 influences synaptic health and contributes to chronic muscle pain.
  • Used fiber photometry and patch-clamp techniques to assess glutamatergic neuronal activity in the dmPFC of CMP rats.
  • Conducted single-cell RNA sequencing to analyze microglial gene expression.
  • Applied optogenetic methods to activate dmPFC glutamatergic neurons and observe effects on pain behavior.
  • Utilized flow cytometry and immunofluorescence to study microglial activation and its impact on neurons.
  • Identified reduced synaptic plasticity and glutamatergic neuronal excitability in the dmPFC of CMP rats.
  • Inhibition of microglia or knockdown of CR3 improved neuronal excitability and synaptic plasticity.
  • Activated DM-PFC neurons alleviated both pain and anxiety-like behaviors in the model.

Cite This Study

Luo et al. (2026) studied this question.

synapsesocial.com/papers/69a67f12f353c071a6f0ae47https://doi.org/10.1038/s12276-026-01666-7
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