ArticleBritish journal of pharmacology2009
Inhibition of human recombinant T-type calcium channels by the endocannabinoid N-arachidonoyl dopamine.
Article in British journal of pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 67 citations in OpenAlex.
- Evaluating FABP5 as a Therapeutic Target for Pain Management.European journal of pain (London, England) · 2026Review
- Interactions Between the Ubiquitin-Proteasome System, Nrf2, and the Cannabinoidome as Protective Strategies to Combat Neurodegeneration: Review on Experimental Evidence.Neurotoxicity research · 2024Review
- Current Drug Development Overview: Targeting Voltage-Gated Calcium Channels for the Treatment of Pain.International journal of molecular sciences · 2023Review
- Central and peripheral contributions of T-type calcium channels in pain.Molecular brain · 2022Review
- Modulation of Recombinant Human T-Type Calcium Channels by ΔCannabis and cannabinoid research · 2022Article
- Capsaicin regulates lipid metabolism through modulation of bile acid/gut microbiota metabolism in high-fat-fed SD rats.Food & nutrition research · 2022Article
- The terpenes camphene and alpha-bisabolol inhibit inflammatory and neuropathic pain via Cav3.2 T-type calcium channels.Molecular brain · 2021Article
- Receptor-Dependent and Independent Regulation of Voltage-Gated CaInternational journal of molecular sciences · 2021Review
- Gut-inhabiting Clostridia build human GPCR ligands by conjugating neurotransmitters with diet- and human-derived fatty acids.Nature microbiology · 2021Article
- Channelopathy of Dravet Syndrome and Potential Neuroprotective Effects of Cannabidiol.Journal of central nervous system disease · 2021Review
- Overexpressed NaFrontiers in cellular neuroscience · 2021Article
- Review
- Analgesic transient receptor potential vanilloid-1-active compounds inhibit native and recombinant T-type calcium channels.British journal of pharmacology · 2019Article
- New approaches and challenges to targeting the endocannabinoid system.Nature reviews. Drug discovery · 2018Review
- Direct Anandamide Activation of TRPV1 Produces Divergent Calcium and Current Responses.Frontiers in molecular neuroscience · 2017Article
- Review
- Identification of N-arachidonoyl dopamine as a highly biased ligand at cannabinoid CB1 receptors.British journal of pharmacology · 2016Article
- NMP-7 inhibits chronic inflammatory and neuropathic pain via block of Cav3.2 T-type calcium channels and activation of CB2 receptors.Molecular pain · 2014Article
- Endothelial atypical cannabinoid receptor: do we have enough evidence?British journal of pharmacology · 2014Review
- 5,6-EET potently inhibits T-type calcium channels: implication in the regulation of the vascular tone.Pflugers Archiv : European journal of physiology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeN-arachidonoyl dopamine (NADA) has complex effects on nociception mediated via cannabinoid CB(1) receptors and the transient receptor potential vanilloid receptor 1 (TRPV1). Anandamide, the prototypic CB(1)/TRPV1 agonist, also inhibits T-type voltage-gated calcium channel currents (I(Ca)). These channels are expressed by many excitable cells, including neurons involved in pain detection and processing. We sought to determine whether NADA and the prototypic arachidonoyl amino acid, N-arachidonoyl glycine (NAGly) modulate T-type I(Ca) EXPERIMENTAL APPROACH: Human recombinant T-type I(Ca) (Ca(V)3 channels) expressed in HEK 293 cells and native mouse T-type I(Ca) were examined using standard whole-cell voltage clamp electrophysiology techniques. KEY
resultsN-arachidonoyl dopamine completely inhibited Ca(V)3 channels with a rank order of potency (pEC(50)) of Ca(V)3.3 (6.45) > or = Ca(V)3.1 (6.29) > Ca(V)3.2 (5.95). NAGly (10 micromol.L(-1)) inhibited Ca(V)3 I(Ca) by approximately 50% or less. The effects of NADA and NAGly were voltage- but not use-dependent, and both compounds produced significant hyperpolarizing shifts in Ca(V)3 channel steady-state inactivation relationships. By contrast with anandamide, NADA and NAGly had modest effects on Ca(V)3 channel kinetics. Both NAGly and NADA inhibited native T-type I(Ca) in mouse sensory neurons. CONCLUSIONS AND IMPLICATIONS: N-arachidonoyl dopamine and NAGly increase the steady-state inactivation of Ca(V)3 channels, reducing the number of channels available to open during depolarization. These effects occur at NADA concentrations at or below to those affecting CB(1) and TRPV1 receptors. Together with anandamide, the arachidonoyl neurotransmitter amides, NADA and NAGly, represent a new family of endogenous T-type I(Ca) modulators.
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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.