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Sensory systems

Chemokines inflame the pain

Nature Reviews Neuroscience volume 4, page 614 (2003)Cite this article

In wild-type mice, mechanical allodynia — a state in which ordinarily non-noxious stimuli cause pain — develops after experimental induction of either neuropathy, by partial ligation of the sciatic nerve, or inflammation, by intraplantar injection of Freund's adjuvant. By contrast, mice lacking CCR2 were not hypersensitive to the same stimuli following the same treatments. This result was specific for chronic pain — there were no differences between wild-type and CCR2-deficient mice, in response to acutely painful stimuli.

These behavioural data indicate that CCR2 participates in the relay of chronic pain signals, but at which point in the processing pathway does it do so? Abbadie et al. used real-time polymerase chain reaction and immunohistochemistry to address this question. In wild-type mice, mechanical allodynia resulting from nerve damage was accompanied by an increase in the number of CCR2-positive monocytes/macrophages, both in the affected nerve and in the dorsal root ganglion. Activated microglia in the spinal cord were also found to express CCR2.

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References

ORIGINAL RESEARCH PAPER

  1. Abbadie, C. et al. Impaired neuropathic pain responses in mice lacking the chemokine receptor CCR2. Proc. Natl Acad Sci. USA 100, 7947–7952 (2003)

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FURTHER READING

  1. Tran, P. B. & Miller, R. J. Chemokine receptors: signposts to brain development and disease. Nature Rev. Neurosci. 4, 444–455 (2003)

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Authors
  1. Suzanne Farley
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Farley, S. Chemokines inflame the pain. Nat Rev Neurosci 4, 614 (2003). https://doi.org/10.1038/nrn1189

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