Effects of Δ9-tetrahydrocannabinol and cannabidiol on phospholipase and other enzymes regulating arachidonate metabolism

White, Helen L.; Tansik, Robert L.

doi:10.1016/0161-4630(80)90049-x

Cited by 38 publications

(18 citation statements)

References 15 publications

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“…1). Two observations are in support of this hypothesis: (1) all authors who have addressed this issue so far agree that LPIs are potent as well as efficacious agonists at GPR55 and (2) both endocannabinoids and THC or synthetic cannabinoids have been found to rapidly activate PLA 2 , not necessarily via interaction with CB 1 or CB 2 receptors, and especially at concentrations higher than 1 μM (White and Tansik 1980;Burstein and Hunter 1981;Evans et al 1987;Burstein et al 1994;Zolese et al 2003;Ambrosi et al 2005;Nabemoto et al 2008). Future studies will have to investigate whether LPIs act as intermediates for endocannabinoid/ phytocannabinoid activation of GPR55 in those experimental conditions in which this effect has been shown.…”

Section: Gpr55mentioning

confidence: 63%

Non-CB1, Non-CB2 Receptors for Endocannabinoids, Plant Cannabinoids, and Synthetic Cannabimimetics: Focus on G-protein-coupled Receptors and Transient Receptor Potential Channels

Petrocellis

Marzo

2009

J Neuroimmune Pharmacol

190

132

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The molecular mechanism of action of Delta(9)-tetrahydrocannabinol (THC), the psychotropic constituent of Cannabis, has been a puzzle during the three decades separating its characterization, in 1964, and the cloning, in the 1990s, of cannabinoid CB1 and CB2 receptors. However, while these latter proteins do mediate most of the pharmacological actions of THC, they do not seem to act as receptors for other plant cannabinoids (phytocannabinoids), nor are they the unique targets of the endogenous lipids that were originally identified in animals as agonists of CB1 and CB2 receptors, and named endocannabinoids. Over the last decade, several potential alternative receptors for phytocannabinoids, endocannabinoids, and even synthetic cannabimimetics, have been proposed, often based uniquely on pharmacological evidence obtained in vitro. In particular, the endocannabinoid anandamide, and the other most abundant Cannabis constituent, cannabidiol, seem to be the most "promiscuous" of these compounds. In this article, we review the latest data on the non-CB1, non-CB2 receptors suggested so far for endocannabinoids and plant or synthetic cannabinoids, and lay special emphasis on uncharacterized or orphan G-protein-coupled receptors as well as on transient receptor potential channels.

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Section: Gpr55mentioning

confidence: 63%

Non-CB1, Non-CB2 Receptors for Endocannabinoids, Plant Cannabinoids, and Synthetic Cannabimimetics: Focus on G-protein-coupled Receptors and Transient Receptor Potential Channels

Petrocellis

Marzo

2009

J Neuroimmune Pharmacol

190

132

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“…Thus, drugs affecting this process, presumably involving PLA 2 , can have a profound effect on the physiological status of a variety of systems. Both CBD and THC produce a significant stimulation of arachidonic acid release in intact human platelets 22 . Interestingly, CBD is roughly 1.5 times more potent than THC suggesting that this action may not be involved in the psychotropic activity of THC.…”

Section: Arachidonic Acid Releasementioning

confidence: 99%

Cannabidiol (CBD) and its analogs: a review of their effects on inflammation

Burstein

2015

Bioorganic & Medicinal Chemistry

461

332

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“…Activation of PLD by cannabinoids depends on cell type. THC stimulated PLD in mouse peritoneal cells [161] and in human platelets [162] while it failed to activate PLD in CHO cells expressing CB 1 [161]. Anandamide activated PLD in PC12 cells but not in NIH 3T3 fibroblasts [163].…”

Section: Arachidonic Acid Metabolismmentioning

confidence: 99%

“…Three enzymes are involved in the release of arachidonic acid from arachidonate derivatives present in the membrane phospholipid domain: phospholipase D, phospholipase C and phospholipase A 2 . The three enzymes have been shown to be activated by cannabinoids [161][162][163][164]. Activation of PLD by cannabinoids depends on cell type.…”

Section: Arachidonic Acid Metabolismmentioning

confidence: 99%

Signal Transduction Activated by Cannabinoid Receptors

Díaz‐Laviada

Ruiz

2005

MRMC

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Since the discovery that cannabinoids exert biological actions through binding to specific receptors, signal mechanisms triggered by these receptors have been focus of extensive study. This review summarizes the current knowledge of the signalling events produced by cannabinoids from membrane receptors to downstream regulators. Two types of cannabinoid receptors have been identified to date: CB(1) and CB(2) both belonging to the heptahelichoidal receptor family but with different tissue distribution and signalling mechanisms. Coupling to inhibitory guanine nucleotide-binding protein and thus inhibition of adenylyl cyclase has been observed in both receptors but other signal transduction pathways that are regulated or not by these G proteins are differently activated upon ligand-receptor binding including ion channels, sphingomyelin hydrolysis, ceramide generation, phospholipases activation and downstream targets as MAP kinase cascade, PI3K, FAK or NOS regulation. Cannabinoids may also act independently of CB(1)or CB(2) receptors. The existence of new unidentified putative cannabinoid receptors has been claimed by many investigators. Endocannabinoids activate vanilloid TRPV1 receptors that may mediate some of the cannabinoid effects. Other actions of cannabinoids can occur through non-receptor-mediated mechanisms.

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Effects of Δ9-tetrahydrocannabinol and cannabidiol on phospholipase and other enzymes regulating arachidonate metabolism

Cited by 38 publications

References 15 publications

Non-CB1, Non-CB2 Receptors for Endocannabinoids, Plant Cannabinoids, and Synthetic Cannabimimetics: Focus on G-protein-coupled Receptors and Transient Receptor Potential Channels

Non-CB1, Non-CB2 Receptors for Endocannabinoids, Plant Cannabinoids, and Synthetic Cannabimimetics: Focus on G-protein-coupled Receptors and Transient Receptor Potential Channels

Cannabidiol (CBD) and its analogs: a review of their effects on inflammation

Signal Transduction Activated by Cannabinoid Receptors

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