ArticleScientific reports2017
Inflammatory and Neuropathic Nociception is Preserved in GPR55 Knockout Mice.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- Minor cannabinoids CBD, CBG, CBN, and CBC differentially modulate sensory neuron activation.The Journal of pharmacology and experimental therapeutics · 2026Article
- Minor Cannabinoids CBD, CBG, CBN and CBC differentially modulate sensory neuron activation.bioRxiv : the preprint server for biology · 2025Article
- Anti-inflammatory effects of hunger are transmitted to the periphery via projection-specific AgRP circuits.Cell reports · 2023Article
- Expression of Cannabinoid Receptors in the Trigeminal Ganglion of the Horse.International journal of molecular sciences · 2023Article
- Peripheral sensory neuron CB2 cannabinoid receptors are necessary for both CB2-mediated antinociceptive efficacy and sparing of morphine tolerance in a mouse model of anti-retroviral toxic neuropathy.Pharmacological research · 2023Article
- Neuronally expressed PDL1, not PD1, suppresses acute nociception.Brain, behavior, and immunity · 2022Article
- Contribution of G Protein-Coupled Receptor 55 to Periaqueductal Gray-Mediated Antinociception in the Inflammatory Pain.Cannabis and cannabinoid research · 2022Article
- GPR55 and GPR119 Receptors Contribute to the Processing of Neuropathic Pain in Rats.Pharmaceuticals (Basel, Switzerland) · 2022Article
- The Cannabidiol Analog PECS-101 Prevents Chemotherapy-Induced Neuropathic Pain via PPARγ Receptors.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022Article
- Computational Approach Reveals Pronociceptive Potential of Cannabidiol in Osteoarthritis: Role of Transient Receptor Potential Channels.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Endocannabinoid signaling pathways: beyond CB1R and CB2R.Journal of cell communication and signaling · 2021Review
- Review
- GPR119 and GPR55 as Receptors for Fatty Acid Ethanolamides, Oleoylethanolamide and Palmitoylethanolamide.International journal of molecular sciences · 2021Review
- Cannabinoids in the descending pain modulatory circuit: Role in inflammation.Pharmacology & therapeutics · 2020Review
- Medial prefrontal cortex diclofenac-induced antinociception is mediated through GPR55, cannabinoid CB1, and mu-opioid receptors of this area and periaqueductal gray.Naunyn-Schmiedeberg's archives of pharmacology · 2020Article
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- Some Prospective Alternatives for Treating Pain: The Endocannabinoid System and Its Putative Receptors GPR18 and GPR55.Frontiers in pharmacology · 2018Review
- Cannabinoid CBThe Journal of pharmacology and experimental therapeutics · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The G-protein coupled receptor GPR55 has been postulated to serve as a novel cannabinoid receptor. A previous report indicated that GPR55 knockout mice fail to develop mechanical hyperalgesia, suggesting a pro-nociceptive role for GPR55 in the control of nociceptive responding. However, GPR55 knockout mice remain incompletely characterized in models of pathological pain. Here we provide a comprehensive assessment of responses of GPR55 knockout and wild-type mice to mechanical and thermal (heat, cold) stimulation in multiple, mechanistically distinct models of inflammatory and neuropathic pain. Inflammatory sensitization was produced by intraplantar administration of capsaicin, formalin or complete Freund's adjuvant. No differences in responding were detected between GPR55 knockout and wild-type mice in any model of inflammatory nociception assessed. Neuropathic pain was induced by partial sciatic nerve ligation (which induces hypersensitivity to mechanical, cold and heat stimulation) or by treatment with the chemotherapeutic agent paclitaxel (which induces hypersensitivity to mechanical and cold stimulation only). No differences were observed between GPR55 knockout and wild type mice in either development or maintenance of neuropathic nociception in either neuropathic pain model. In conclusion, genetic deletion of GPR55 did not alter the development of pathological pain in adult mice in any chronic pain model evaluated.
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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.