Spinal microglia contribute to sustained inflammatory pain via amplifying neuronal activity

Nan Gu, Min Hee Yi, Madhuvika Murugan, Manling Xie, Sebastian Parusel, Jiyun Peng, Ukpong B. Eyo, Christine L. Hunt, Hailong Dong, Long Jun Wu

Research output: Contribution to journalArticlepeer-review

Abstract

Microglia are highly dynamic immune cells of the central nervous system (CNS). Microglial processes interact with neuronal elements constantly on the order of minutes. The functional significance of this acute microglia-neuron interaction and its potential role in the context of pain is still largely unknown. Here, we found that spinal microglia increased their process motility and electrophysiological reactivity within an hour after the insult in a mouse model of formalin-induced acute, sustained, inflammatory pain. Using an ablation strategy to specifically deplete resident microglia in the CNS, we demonstrate that microglia participate in formalin-induced acute sustained pain behaviors by amplifying neuronal activity in the spinal dorsal horn. Moreover, we identified that the P2Y12 receptor, which is specifically expressed in microglia in the CNS, was required for microglial function in formalin-induced pain. Taken together, our study provides a novel insight into the contribution of microglia and the P2Y12 receptor in inflammatory pain that could be used for potential therapeutic strategies.

Original languageEnglish (US)
Article number86
JournalMolecular Brain
Volume15
Issue number1
DOIs
StatePublished - Dec 2022

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Cellular and Molecular Neuroscience

Keywords

  • Formalin
  • Inflammatory pain
  • Microglia
  • Microglia–neuron interaction
  • P2Y12 receptor
  • Two-photon imaging

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