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. 2019 Nov 12;12:273. doi: 10.3389/fnmol.2019.00273

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Copyright © 2019 Retamal, Ramírez-García, Shenoy, Poole and Veldhuis.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Role of G protein-coupled receptors (GPCRs) in pain and neurogenic inflammation. Injury or damaged tissues and infiltrating immune cells stimulate GPCRs on the peripheral sensory nerve terminals through release of painful and inflammatory mediators. Activated peptidergic and non-peptidergic Aδ and C fibers contribute to the response via the release of glutamate, Substance P (SP) and Calcitonin Gene-Related Peptide (CGRP) at the injury site and central terminals. The presence of endogenous mediators in the spinal cord (neuro- and glio-transmitters) can promote activation and recycling of GPCRs including pre-synaptic CB_1/2 cannabinoid and Mu-opioid receptor (MOR)/Delta-opioid receptor (DOR) and the exocytic trafficking of the γ-aminobutyric acid_A receptor (GABAR) which is an inhibitory receptor that can normalize neuronal excitability where excitatory neurotransmitters are released. Stimulation and endocytosis of receptors such as Neurokinin 1 Receptor (NK₁R) and Calcitonin Receptor-Like Receptor/Receptor Activity-Modifying Protein 1 (CLR/RAMP1) in post-synaptic neurons are known to modify firing frequency and the duration of pain responses (Jensen et al., 2017; Yarwood et al., 2017; Stoeber et al., 2018).