Interaction of brain cannabinoid receptors with guanine nucleotide binding protein

Petitet, François; Jeantaud, Bernadette; Capet, Marc; Doble, Adam

doi:10.1016/s0006-2952(97)00384-5

Cited by 21 publications

(17 citation statements)

References 7 publications

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“…35 S] GTPγS binding to membranes obtained from rat cerebellum or rat or mouse whole brain (Burkey et al 1997;Leggett et al 2004;Petitet et al 1997;Savinainen et al 2001). Finally, docosahexaenoylethanolamide and eicosapentaenoylethanolamide each appear to stimulate […”

Section: [ 35 S]gtpgs Binding Assaymentioning

confidence: 99%

Endocannabinoids and Their Pharmacological Actions

Pertwee

2015

Handbook of Experimental Pharmacology

250

235

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The endocannabinoid system consists of G protein-coupled cannabinoid CB(1) and CB(2) receptors, of endogenous compounds known as endocannabinoids that can target these receptors, of enzymes that catalyse endocannabinoid biosynthesis and metabolism, and of processes responsible for the cellular uptake of some endocannabinoids. This review presents in vitro evidence that most or all of the following 13 compounds are probably orthosteric endocannabinoids since they have all been detected in mammalian tissues in one or more investigation, and all been found to bind to cannabinoid receptors, probably to an orthosteric site: anandamide, 2-arachidonoylglycerol, noladin ether, dihomo-γ-linolenoylethanolamide, virodhamine, oleamide, docosahexaenoylethanolamide, eicosapentaenoylethanolamide, sphingosine, docosatetraenoylethanolamide, N-arachidonoyldopamine, N-oleoyldopamine and haemopressin. In addition, this review describes in vitro findings that suggest that the first eight of these compounds can activate CB(1) and sometimes also CB(2) receptors and that another two of these compounds are CB(1) receptor antagonists (sphingosine) or antagonists/inverse agonists (haemopressin). Evidence for the existence of at least three allosteric endocannabinoids is also presented. These endogenous compounds appear to target allosteric sites on cannabinoid receptors in vitro, either as negative allosteric modulators of the CB1 receptor (pepcan-12 and pregnenolone) or as positive allosteric modulators of this receptor (lipoxin A(4)) or of the CB(2) receptor (pepcan-12). Also discussed are current in vitro data that indicate the extent to which some established or putative orthosteric endocannabinoids seem to target non-cannabinoid receptors and ion channels, particularly at concentrations at which they have been found to interact with CB(1) or CB(2) receptors.

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Section: [ 35 S]gtpgs Binding Assaymentioning

confidence: 99%

Endocannabinoids and Their Pharmacological Actions

Pertwee

2015

Handbook of Experimental Pharmacology

250

235

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“…Of these, (-)-∆ 8 -THC resembles (-)-∆ 9 -THC both in its CB 1 and CB 2 receptor affinities (Table 2) and in its relative intrinsic activity at the CB 1 receptor (Gérard et al 1991;Howlett and Fleming 1984;Matsuda et al 1990). Cannabinol also behaves as a partial agonist at CB 1 receptors but has even less relative intrinsic activity than (-)-∆ 9 -THC (Howlett 1987;Matsuda et al 1990;Petitet et al 1997Petitet et al , 1998. Whilst there is one report that cannabinol activates CB 2 receptors in the cyclic AMP assay more effectively than ∆ 9 -THC (Rhee et al 1997), there is another that in the GTPγS binding assay, it behaves as a CB 2 receptor inverse agonist (MacLennan et al 1998).…”

Section: Cannabinoid Receptor Agonistsmentioning

confidence: 99%

Pharmacological Actions of Cannabinoids

Pertwee

Handbook of Experimental Pharmacology

502

515

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“…Despite various papers described SR141716A as an antagonist [56][57][58], today this compound is considered to act as an inverse agonist based on [ 35 S]-GTPγ S [59][60][61][62] and cAMP accumulation assays [62][63][64] (Table 2). An interesting review dealing with inverse agonism at the cannabinoid receptors, and mostly with SR141716A effects, was recently published by Roger Pertwee [65].…”

Section: Diarylpyrazole Derivativesmentioning

confidence: 99%

Current Knowledge on the Antagonists and Inverse Agonists of Cannabinoid Receptors

Muccioli¹,

Lambert

2005

CMC

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Ten years elapsed since the discovery by Sanofi of SR141716A the first selective CB(1) cannabinoid receptor antagonist. Shortly after, Sanofi also reported the synthesis of the first selective CB(2) cannabinoid receptor antagonist, SR144528. Since these two milestones in the cannabinoid field, many other compounds, more or less related to the Sanofi compounds, or based on a completely different scaffold appeared. Several of these compounds are currently involved in clinical trials for diseases such as obesity, nicotine and alcohol addictions, or allergies. Further, the cannabinoid receptors knock-out mice production strengthened the hypothesis of the existence of several other "cannabinoid" receptors for which the first antagonists begin to appear. The large amount of patents taken by many different pharmaceutical companies prove, if necessary, the great therapeutic potential expected for the cannabinoid receptors antagonists.

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Interaction of brain cannabinoid receptors with guanine nucleotide binding protein

Cited by 21 publications

References 7 publications

Endocannabinoids and Their Pharmacological Actions

Endocannabinoids and Their Pharmacological Actions

Pharmacological Actions of Cannabinoids

Current Knowledge on the Antagonists and Inverse Agonists of Cannabinoid Receptors

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