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Updated: Jan 23, 2026

Chronic Constriction Injury of the Rat's Infraorbital Nerve IoN-CCI to Study Trigeminal Neuropathic Pain
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Chronic Constriction Injury of the Rat's Infraorbital Nerve IoN-CCI to Study Trigeminal Neuropathic Pain

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Microglia in the Primary Somatosensory Barrel Cortex Mediate Trigeminal Neuropathic Pain

Yuping Wang1, Peng Cao1, Lisheng Mei1

  • 1Hefei National Laboratory for Physical Sciences at the Microscale, Key Laboratory of Brain Function and Disease, Department of Biophysics and Neurobiology, University of Science and Technology of China, Hefei 230027, PR China.

Neuroscience
|June 11, 2019
PubMed

Insights

Microglia in the brain

Area of Science:

  • Neuroscience
  • Pain Research
  • Cellular Biology

Background:

  • Trigeminal neuropathic pain (TGN) is a severe headache condition with unclear neural mechanisms.
  • Abnormal cortical activity is implicated in TGN, but specific cellular roles are largely unknown.

Purpose of the Study:

  • To investigate the role of microglia in the primary somatosensory barrel cortex (S1BF) in a mouse model of TGN.
  • To explore the relationship between microglial activation and neuronal hyperactivity in TGN.

Main Methods:

  • Electrophysiological recordings were used to assess neuronal activity in the S1BF.
  • Chemogenetics was employed to manipulate glutamatergic neuron activity in the S1BF.
  • Minocycline, a microglia inhibitor, was administered to evaluate its effects on pain and neuronal activity.

Main Results:

  • Significant neuronal hyperactivity was observed in glutamatergic neurons of the S1BF (GluS1BF) in TGN mice.
  • Inhibition of GluS1BF neurons reduced pain behaviors, while activation induced pain sensitization.
  • Microglia in the S1BF (microgliaS1BF) showed activation, with altered density and morphology.
  • Minocycline treatment attenuated pain sensitization and reduced GluS1BF neuronal activity.

Conclusions:

  • Microglia in the S1BF play a critical role in regulating trigeminal neuropathic pain.
  • Microglial activation influences glutamatergic neuronal adaptation in the S1BF, contributing to TGN pathogenesis.
  • Targeting microglia may offer a therapeutic strategy for managing TGN.
Keywords:
Chronic constriction injuryglutamatergic neuronsmicrogliatrigeminal neuropathic pain

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