ArticleNeuroscience letters2013
CB1 cannabinoid receptor agonist prevents NGF-induced sensitization of TRPV1 in sensory neurons.
Article in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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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.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- FABP5 deletion in nociceptors augments endocannabinoid signaling and suppresses TRPV1 sensitization and inflammatory pain.Scientific reports · 2022Trial
- The Endocannabinoid System in Endometriosis-Associated Pain: Mechanisms, Molecular Targets, and Therapeutic Implications.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- Electroacupuncture alleviates zymosan-induced colorectal hypersensitivity.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025Article
- The Development of Cannabinoids as Therapeutic Agents in the United States.Pharmacological reviews · 2024Review
- Joint CB1 and NGF Receptor Activation Suppresses TRPM8 Activation in Etoposide-Resistant Retinoblastoma Cells.International journal of molecular sciences · 2024Article
- The dual role of TRPV1 in peripheral neuropathic pain: pain switches caused by its sensitization or desensitization.Frontiers in molecular neuroscience · 2024Review
- Cannabinoid-Based Ocular Therapies and Formulations.Pharmaceutics · 2023Review
- The Cannabinoid Ligand Arachidonyl-2'-Chloroethylamide (ACEA) Ameliorates Depressive and Overactive Bladder Symptoms in a Corticosterone-Induced Female Wistar Rat Model.International journal of molecular sciences · 2023Article
- Intrathecal administration of Resolvin D1 and E1 decreases hyperalgesia in mice with bone cancer pain: Involvement of endocannabinoid signaling.Prostaglandins & other lipid mediators · 2020Article
- Allosteric Cannabinoid Receptor 1 (CB1) Ligands Reduce Ocular Pain and Inflammation.Molecules (Basel, Switzerland) · 2020Article
- Potential for endocannabinoid system modulation in ocular pain and inflammation: filling the gaps in current pharmacological options.Neuronal signaling · 2018Review
- The Cannabinoids ΔCannabis and cannabinoid research · 2018Article
- Immunolocalization of cannabinoid receptor type 1 and CB2 cannabinoid receptors, and transient receptor potential vanilloid channels in pterygium.Molecular medicine reports · 2017Article
- Neurotrophins and Neuropathic Pain: Role in Pathobiology.Molecules (Basel, Switzerland) · 2015Review
- Cannabinoid receptor type 1 antagonist, AM251, attenuates mechanical allodynia and thermal hyperalgesia after burn injury.Anesthesiology · 2014Article
- Social stress induces changes in urinary bladder function, bladder NGF content, and generalized bladder inflammation in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2014Article
- Glucose concentration in culture medium affects mRNA expression of TRPV1 and CB1 receptors and changes capsaicin toxicity in PC12 cells.Iranian journal of basic medical sciences · 2014Article
- Peripheral gating of pain signals by endogenous lipid mediators.Nature neuroscience · 2014Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The transient receptor potential vanilloid type 1 channel (TRPV1) and nerve growth factor (NGF) are important mediators of inflammatory pain. NGF released during inflammation sensitizes TRPV1 in afferent nerve endings of peripheral nociceptors, increasing pain sensation. Cannabinoids, by activating CB1 G protein-coupled receptors, produce analgesia in a variety of pain models, though the exact mechanisms are not known. We tested the hypothesis that activation of the CB1 receptor by cannabinoids attenuates NGF-induced TRPV1 sensitization. TRPV1-mediated currents were measured in acutely isolated primary sensory neurons with the whole-cell patch clamp technique using capsaicin (100 nM) as the agonist. After the first capsaicin application, during which the baseline current was measured, cells were exposed to NGF (100 ng/mL), and the capsaicin application was repeated after 5 min. NGF sensitized TRPV1 in 31.0% of cells (13 of 42), with a mean (±SE) increase in the capsaicin-induced current of 262 ± 47% over the baseline current. When the cannabinoid agonist ACEA (arachidonoyl-2'-chloroethylamide; 10nM) was given before NGF, only 10.8% of cells (4 of 37) were sensitized (p<0.05). Neither this rate, nor the magnitude of the sensitization (198 ± 63% of baseline) were different from that seen in cells not treated with NGF (3 of 25 cells sensitized (12.0%), 253 ± 70% of baseline). Pretreatment with the CB1 antagonist AM-251 (100 nM) prevented the effect of ACEA on NGF-induced sensitization. These results support the hypothesis that cannabinoids, acting through CB1 receptors, may produce analgesia in part by preventing NGF-induced sensitization of TRPV1 in afferent nociceptor nerve endings.
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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.