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Author Spotlight: Microglia Research on Spinal Cord Heterogeneity and Purification
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Microglia Are Indispensable for Synaptic Plasticity in the Spinal Dorsal Horn and Chronic Pain

Li-Jun Zhou1, Jiyun Peng2, Ya-Nan Xu3

  • 1Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou 510080, China; Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ 08854, USA; Guangdong Province Key Laboratory of Brain Function and Disease, Guangzhou 510080, China.

Cell Reports
|June 27, 2019
PubMed

Insights

Spinal long-term potentiation (LTP) can cause chronic pain by altering nerve pathways. Microglia-driven signaling involving colony-stimulating factor 1 (CSF-1) and brain-derived neurotrophic factor (BDNF) is crucial for this pain transition.

Area of Science:

  • Neuroscience
  • Pain Research
  • Cell Biology

Background:

  • Spinal long-term potentiation (LTP) at C-fiber synapses is a proposed mechanism for chronic pain.
  • A direct causal link between spinal LTP and chronic pain has not been established.

Purpose of the Study:

  • To investigate the causal relationship between spinal LTP and the development of chronic pain.
  • To identify the molecular mechanisms, particularly involving microglia, that mediate spinal LTP and chronic pain.

Main Methods:

  • Induction of spinal LTP in mice via high-frequency stimulation (HFS) of the sciatic nerve.
  • Assessment of chronic pain behaviors, CGRP terminal changes, and microglial activation.
  • Pharmacological and genetic manipulations, including NMDA receptor blockade, microglial ablation, and conditional deletion of microglial BDNF, as well as antibody inhibition of CSF-1.

Main Results:

  • HFS reliably induced spinal LTP and chronic pain lasting over 35 days without nerve injury.
  • HFS increased calcitonin gene-related peptide (CGRP) terminals in the spinal dorsal horn.
  • Blocking NMDA receptors, ablating microglia, or deleting microglial BDNF prevented pain and morphological changes.
  • Antibodies against colony-stimulating factor 1 (CSF-1) inhibited HFS-induced LTP, microglial activation, and BDNF upregulation.

Conclusions:

  • Microglial CSF-1 and BDNF signaling are essential for spinal LTP and chronic pain development.
  • Microglia-dependent synaptic potentiation transitions to structural alterations in pain pathways, potentially underlying pain chronicity.
Keywords:
brain-derived neurotrophic factorcalcitonin gene-related peptidechronic paincolony-stimulating factor 1high-frequency stimulationlong-term potentiationmicroglia

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