Complement 3a receptor in dorsal horn microglia mediates pronociceptive neuropeptide signaling

Suzanne Doolen, Jennifer Cook, Maureen Riedl, Kelley Kitto, Shinichi Kohsaka, Christopher N. Honda, Carolyn A. Fairbanks, Bradley K. Taylor, Lucy Vulchanova

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


The complement 3a receptor (C3aR1) participates in microglial signaling under pathological conditions and was recently shown to be activated by the neuropeptide TLQP-21. We previously demonstrated that TLQP-21 elicits hyperalgesia and contributes to nerve injury-induced hypersensitivity through an unknown mechanism in the spinal cord. Here we determined that this mechanism requires C3aR1 and that microglia are the cellular target for TLQP-21. We propose a novel neuroimmune signaling pathway involving TLQP-21-induced activation of microglial C3aR1 that then contributes to spinal neuroplasticity and neuropathic pain. This unique dual-ligand activation of C3aR1 by a neuropeptide (TLQP-21) and an immune mediator (C3a) represents a potential broad-spectrum mechanism throughout the CNS for integration of neuroimmune crosstalk at the molecular level.

Original languageEnglish (US)
Pages (from-to)1976-1989
Number of pages14
Issue number12
StatePublished - Dec 2017

Bibliographical note

Publisher Copyright:
© 2017 Wiley Periodicals, Inc.


  • calcium imaging
  • neuroimmune
  • pain


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