ArticleMolecular pain2015
Attenuation of inflammatory and neuropathic pain behaviors in mice through activation of free fatty acid receptor GPR40.
Article in Molecular pain, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 41 citations in OpenAlex.
- Metabolite-Sensing Receptors: Emerging Targets for Modulating Chronic Pain Pathways.Current issues in molecular biology · 2025Review
- Anti-Inflammatory and Antinociceptive Properties of the Quercetin-3-Oleate AV2, a Novel FFAR1 Partial Agonist.International journal of molecular sciences · 2024Article
- Vincamine as an agonist of G-protein-coupled receptor 40 effectively ameliorates diabetic peripheral neuropathy in mice.Acta pharmacologica Sinica · 2023Article
- The role of free fatty acid receptor pathways in a selective regulation of TRPA1 and TRPV1 by resolvins in primary sensory neurons.Journal of cellular physiology · 2022Article
- Genetic Inactivation of Free Fatty Acid Receptor 3 Impedes Behavioral Deficits and Pathological Hallmarks in the APPInternational journal of molecular sciences · 2022Article
- Glycosides for Peripheral Neuropathic Pain: A Potential Medicinal Components.Molecules (Basel, Switzerland) · 2021Review
- FFAR1/GPR40 Contributes to the Regulation of Striatal Monoamine Releases and Facilitation of Cocaine-Induced Locomotor Activity in Mice.Frontiers in pharmacology · 2021Article
- Nonesterified Fatty Acids and Depression in Cancer Patients and Caregivers.Current developments in nutrition · 2020Article
- Aging-Related Phenotypic Conversion of Medullary Microglia Enhances Intraoral Incisional Pain Sensitivity.International journal of molecular sciences · 2020Article
- Activation of GPR40 produces mechanical antiallodynia via the spinal glial interleukin-10/β-endorphin pathway.Journal of neuroinflammation · 2019Article
- TAK-875 MitigatesJournal of diabetes research · 2019Article
- Fatty Acid Signaling Mechanisms in Neural Cells: Fatty Acid Receptors.Frontiers in cellular neuroscience · 2019Review
- Integrated Analysis of DNA Methylation and Biochemical/Metabolic Parameter During the Long-Term Isolation Environment.Frontiers in physiology · 2019Article
- Oxidized Lipids in Persistent Pain States.Frontiers in pharmacology · 2019Review
- GPR40 modulates epileptic seizure and NMDA receptor function.Science advances · 2018Article
- Dyslipidemia impairs mitochondrial trafficking and function in sensory neurons.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
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- New paradigms in GPCR drug discovery.Biochemical pharmacology · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe G-protein-coupled receptor 40 (GPR40) is suggested to function as a transmembrane receptor for medium- to long-chain free fatty acids and is implicated to play a role in free fatty acids-mediated enhancement of glucose-stimulated insulin secretion from pancreas. However, the functional role of GPR40 in nervous system including somatosensory pain signaling has not been fully examined yet.
resultsIntrathecal injection of GPR40 agonist (MEDICA16 or GW9508) dose-dependently reduced ipsilateral mechanical allodynia in CFA and SNL models and thermal hyperalgesia in carrageenan model. These anti-allodynic and anti-hyperalgesic effects were almost completely reversed by a GPR40 antagonist, GW1100. Immunohistochemical analysis revealed that GPR40 is expressed in spinal dorsal horn and dorsal root ganglion neurons, and immunoblot analysis showed that carrageenan or CFA inflammation or spinal nerve injury resulted in increased expression of GPR40 in these areas. Patch-clamp recordings from spinal cord slices exhibited that bath-application of either MEDICA16 or GW9508 significantly decreased the frequency of spontaneous excitatory postsynaptic currents in the substantia gelatinosa neurons of the three pain models.
conclusionsOur results indicate that GPR40 signaling pathway plays an important suppressive role in spinal nociceptive processing after inflammation or nerve injury, and that GPR40 agonists might serve as a new class of analgesics for treating inflammatory and neuropathic pain.
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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.