Complement 3a receptor in dorsal horn microglia mediates pronociceptive neuropeptide signaling
Year: 2017
Type: article
Abstract: 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.
Source: Glia
DOI: 10.1002/glia.23208
Language: English
Subfield: Physiology
Field: Medicine
Domain: Health Sciences
Open Access status: green
Awards: Glutamate Receptor Modulation of Calcium Signaling in Neuropathic Pain, Predoctoral Training of Neuroscientists, TLQP-21 and C3aR, a Novel Receptor/Ligand Interaction in Neuropathic Pain, Contribution of TLQP21 and its receptor C3aR1 to neuropathic pain after spinal cord injury, Long-term activation of spinal opioid analgesia after inflammation, Neuroscience Training in Drug Abuse Research
OpenAlex ID: W2752873771