ReviewPharmacology & therapeutics2008
Modulation of pain transmission by G-protein-coupled receptors.
Review in Pharmacology & therapeutics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 102 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
102 citing papers in PubMed, 1 synthesis or guideline pooled it, 193 citations in OpenAlex.
- Psychopharmacological Therapy Positively Modulates Disease Activity in Inflammatory Bowel Disease: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Targeting GCell reports. Medicine · 2026Article
- From tooth pain to trigeminal sensitization: translational models, experimental readouts, and mechanism-guided therapeutic opportunities in odontogenic and headache-related orofacial pain.The journal of headache and pain · 2026Review
- GABAExperimental physiology · 2026Article
- Article
- Novel GαGTP Sensors Reveal Endogenous and Subcellular G Protein Signaling Dynamics.bioRxiv : the preprint server for biology · 2026Article
- The Translational Biology of Temporomandibular Disorder Pain: Mechanisms, Biomarkers, and Therapeutic Perspectives.Journal of pain research · 2026Review
- Suppression of neuropathic pain hypersensitivity by TRPM8 is mediated by mGluR group II and III receptors acting differentially on distinct nociceptor inputs to spinal cord.Frontiers in pharmacology · 2026Article
- GαScience signaling · 2025Article
- Multimodal Analgesia in Cardiothoracic Procedure: Opioid and Non-opioid Pharmacology for Pain Management: Part 1.Annals of cardiac anaesthesia · 2025Review
- GABAJournal of neurochemistry · 2025Article
- Impaired modulation of the trigeminal caudal nucleus by the locus coeruleus in diabetic mice: the role of GABAergic and glycinergic neurons.Frontiers in neuroanatomy · 2025Article
- Modulation of Brain-derived Neurotrophic Factor Expression by Physical Exercise in Reserpine-induced Pain-depression Dyad in Mice.Experimental neurobiology · 2024Article
- Get Ready to Sharpen Your Tools: A Short Guide to Heterotrimeric G Protein Activity Biosensors.Molecular pharmacology · 2024Review
- Calcium-sensing receptor regulates Kv7 channels via GBritish journal of pharmacology · 2024Article
- Cannabinoid Analgesia in Postoperative Pain Management: From Molecular Mechanisms to Clinical Reality.International journal of molecular sciences · 2024Review
- Integration of selective sweeps across the sheep genome: understanding the relationship between production and adaptation traits.Genetics, selection, evolution : GSE · 2024Article
- Evaluation of New Approaches to Depression Treatment Using an Animal Model of Pharmacoresistant Depression.International journal of molecular sciences · 2024Article
- The role of orphan G protein-coupled receptors in pain.Heliyon · 2024Review
- Repurposing EGFR Inhibitors for Oral Cancer Pain and Opioid Tolerance.Pharmaceuticals (Basel, Switzerland) · 2023Review
42 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
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, alpha2-adrenergic, muscarinic acetylcholine, gamma-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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.