ArticleBritish journal of pharmacology2016
Identification of N-arachidonoyl dopamine as a highly biased ligand at cannabinoid CB1 receptors.
Article in British journal of pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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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
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Cannabinoid Receptors: An Update on Cell Signaling, Pathophysiological Roles and Therapeutic Opportunities in Neurological, Cardiovascular, and Inflammatory Diseases.International journal of molecular sciences · 2020Pooled it
- The PM20D1-NADA pathway protects against Parkinson's disease.Cell death and differentiation · 2024Article
- GPR55 Receptor Activation by theInternational journal of molecular sciences · 2021Article
- Molecular Pharmacology of Synthetic Cannabinoids: Delineating CB1 Receptor-Mediated Cell Signaling.International journal of molecular sciences · 2020Review
- The Endocannabinoid System May Modulate Sleep Disorders in Aging.Current neuropharmacology · 2020Review
- Cannabichromene is a cannabinoid CBBritish journal of pharmacology · 2019Article
- Selective modulation of the cannabinoid type 1 (CBMedChemComm · 2019Review
- Structural Insights into CB1 Receptor Biased Signaling.International journal of molecular sciences · 2019Review
- Modulation of the Endocannabinoid System as a Potential Anticancer Strategy.Frontiers in pharmacology · 2019Review
- Review
- Approaches to Assess Biased Signaling at the CB1R Receptor.Methods in enzymology · 2017Article
- Cannabinoid CBCannabis and cannabinoid research · 2017Review
- Affinity and Efficacy Studies of Tetrahydrocannabinolic Acid A at Cannabinoid Receptor Types One and Two.Cannabis and cannabinoid research · 2017Article
- Identification of N-arachidonoyl dopamine as a highly biased ligand at cannabinoid CB1 receptors.British journal of pharmacology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeN-arachidonyl dopamine (NADA) has been identified as a putative endocannabinoid, but there is little information about which signalling pathways it activates. The purpose of this study was to identify the signalling pathways activated by NADA in vitro. EXPERIMENTAL APPROACH: Human or rat cannabinoid CB1 receptors were expressed in AtT20, CHO or HEK 293 cells. NADA displacement of radiolabelled cannabinoids, and CB1 receptor mediated activation of K channels or ERK phosphorylation, release of intracellular calcium ([Ca]i ) and modulation of adenylyl cyclase were measured in addition to NADA effects on CB1 receptor trafficking. KEY
resultsAt concentrations up to 30 μM, NADA failed to activate any signalling pathways via CB1 receptors, with the exception of mobilization of [Ca]i . The elevations of [Ca]i were insensitive to pertussis toxin, and reduced or abolished by blockers of Gq /11 -dependent processes including U73122, thapsigargin and a peptide antagonist of Gq /11 activation. Prolonged NADA incubation produced modest loss of cell surface CB1 receptors. The prototypical cannabinoid agonist CP55940 signalled as expected in all assays. CONCLUSIONS AND IMPLICATIONS: NADA is an ineffective agonist at most canonical cannabinoid receptor signalling pathways, but did promote mobilization of [Ca]i via Gq -dependent processes and some CB1 receptor trafficking. This signalling profile is distinct from that of any known cannabinoid, and suggests that NADA may have a unique spectrum of effects in vivo. Our results also indicate that it may be possible to identify highly biased CB1 receptor ligands displaying a subset of the pharmacological or therapeutic effects usually attributed to CB1 ligands.
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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.