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Characterization and Isolation of Mouse Primary Microglia by Density Gradient Centrifugation
Published on: February 16, 2018
Infant nerve injury induces delayed microglial polarization to the M1 phenotype, and exercise reduces delayed
Xingrui Gong1, Yongmei Chen2, Bao Fu3
1Department of Anesthesiology and Pediatric Clinical Pharmacology Laboratory, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai, China; Department of Anesthesiology, Shiyan Taihe Hospital (affiliated Hospital of Hubei University of Medicine), Shiyan, Hubei, China.
Abstract:
Neuropathic pain is absent in infants and emergent years after injury. Adult spinal cord microglia play a key role in initiating neuropathic pain, and modulation of microglia is a potential target for treating neuropathic pain. In this study, we evaluated the role of microglia after infant peripheral nerve injury and the effect of exercise on the delayed-onset neuropathic pain. Rat pups received spared nerve injury, and behavior tests were performed to evaluate their pain threshold. qPCR, immunohistochemistry, and Western blot were used for M1 and M2 marker expression analysis. In contrast to the microglial polarization to the M1 phenotype observed in the adult spinal cord, in infant nerve injury, microglial polarization immediately shifted to the M2 phenotype. In adolescence, microglia polarized to the M1 phenotype, which was concomitant with the emergence of neuropathic pain. Exercise shifted spinal cord microglia polarization to the M2 phenotype and reduced neuropathic pain. In addition, IL-10 increased and TNF-α decreased after exercise, and intrathecal injection of the IL-10 antibody reduced the exercise-induced analgesia. Our study found that infant nerve injury induced delayed spinal cord microglia polarization to the M1 phenotype and that exercise was effective in the treatment of delayed adolescent neuropathic pain via the modulation of microglial polarization.
Insights
Infant nerve injury causes delayed neuropathic pain in rats by altering spinal cord microglia. Exercise effectively treats this pain by shifting microglia to an anti-inflammatory M2 state.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Adult spinal cord microglia are crucial in initiating neuropathic pain.
- Microglia modulation offers a potential therapeutic target for neuropathic pain.
Purpose of the Study:
- To investigate the role of microglia in infant peripheral nerve injury.
- To assess the impact of exercise on delayed-onset neuropathic pain in adolescent rats.
Main Methods:
- Rat pups underwent spared nerve injury.
- Behavioral tests evaluated pain thresholds.
- qPCR, immunohistochemistry, and Western blot analyzed M1/M2 microglial markers.
Main Results:
- Infant injury caused immediate M2 microglial polarization, unlike adult M1 polarization.
- Adolescence saw M1 polarization and neuropathic pain onset.
- Exercise promoted M2 polarization, reduced pain, increased IL-10, and decreased TNF-α.
Conclusions:
- Infant nerve injury leads to delayed M1 microglial polarization in the spinal cord.
- Exercise effectively treats adolescent neuropathic pain by modulating microglial polarization.
