TY - JOUR
T1 - Modulation of pain transmission by G-protein-coupled receptors
AU - Pan, Hui Lin
AU - Wu, Zi Zhen
AU - Zhou, Hong Yi
AU - Chen, Shao Rui
AU - Zhang, Hong Mei
AU - Li, De Pei
N1 - Funding Information:
Work conducted in the authors' laboratory was supported by grants GM64830 and NS45602 from the National Institutes of Health.
PY - 2008/1
Y1 - 2008/1
N2 - The heterotrimeric G-protein-coupled receptors (GPCR) represent the largest and most diverse family of cell surface receptors and proteins. GPCR are widely distributed in the peripheral and central nervous systems and are one of the most important therapeutic targets in pain medicine. GPCR are present on the plasma membrane of neurons and their terminals along the nociceptive pathways and are closely associated with the modulation of pain transmission. GPCR that can produce analgesia upon activation include opioid, cannabinoid, α2-adrenergic, muscarinic acetylcholine, γ-aminobutyric acidB (GABAB), groups II and III metabotropic glutamate, and somatostatin receptors. Recent studies have led to a better understanding of the role of these GPCR in the regulation of pain transmission. Here, we review the current knowledge about the cellular and molecular mechanisms that underlie the analgesic actions of GPCR agonists, with a focus on their effects on ion channels expressed on nociceptive sensory neurons and on synaptic transmission at the spinal cord level.
AB - The heterotrimeric G-protein-coupled receptors (GPCR) represent the largest and most diverse family of cell surface receptors and proteins. GPCR are widely distributed in the peripheral and central nervous systems and are one of the most important therapeutic targets in pain medicine. GPCR are present on the plasma membrane of neurons and their terminals along the nociceptive pathways and are closely associated with the modulation of pain transmission. GPCR that can produce analgesia upon activation include opioid, cannabinoid, α2-adrenergic, muscarinic acetylcholine, γ-aminobutyric acidB (GABAB), groups II and III metabotropic glutamate, and somatostatin receptors. Recent studies have led to a better understanding of the role of these GPCR in the regulation of pain transmission. Here, we review the current knowledge about the cellular and molecular mechanisms that underlie the analgesic actions of GPCR agonists, with a focus on their effects on ion channels expressed on nociceptive sensory neurons and on synaptic transmission at the spinal cord level.
KW - Analgesia
KW - Dorsal root ganglion
KW - G-protein-coupled inwardly rectifying K channels
KW - Spinal cord
KW - Synaptic transmission
KW - Voltage-gated Ca channels
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U2 - 10.1016/j.pharmthera.2007.09.003
DO - 10.1016/j.pharmthera.2007.09.003
M3 - Review article
C2 - 17959251
AN - SCOPUS:36549075610
SN - 0163-7258
VL - 117
SP - 141
EP - 161
JO - Pharmacology and Therapeutics
JF - Pharmacology and Therapeutics
IS - 1
ER -