Disease relevance of Noladin

• 5 In mesenteric beds from pertussis toxin (PTX)-pretreated rats, the inhibitory actions of noladin ether on sensory neurotransmission were abolished, indicating the involvement of G(i/o) protein-coupled receptors [1].
• Anandamide and noladin ether, at nanomolar concentrations, showed concentration dependent inhibition of Abeta toxicity [2].
• Thus, Noladin could be of potential clinical benefit in treating disorders of body weight [3].
• These results indicate that Noladin has a significant dose-dependent effect on food consumption, cognition and weight maintenance after weight loss [3].

Psychiatry related information on Noladin

• Effects of the endocannabinoid noladin ether on body weight, food consumption, locomotor activity, and cognitive index in mice [3].

High impact information on Noladin

• Noladin ether (a stable 2-AG analog) and exogenous CB1 receptor agonists possess similar effects [4].
• The CB1 receptor agonist noladin ether was inactive [5].
• RESULTS: Within 1 hour after adding 3, 30, or 300 nM of noladin ether, the aqueous humor outflow facility increased concentration dependently [6].
• Furthermore, noladin ether treatment caused rounding of trabecular meshwork cells, and there was a decrease of actin stress fibers, as well as a decrease in focal adhesions [6].
• The effect of 30 nM of noladin ether was completely blocked by SR141716A, a selective CB1 antagonist [6].

Biological context of Noladin

• The monophosphate ester of noladin ether reduced intraocular pressure in normotensive rabbits [7].
• Noladin ether (1 microm) reduced vasorelaxation at a submaximal frequency (8 Hz), from 57.3+/-6.8 to 23.3+/-3.8% (P<0.05, n=4) [1].
• Forskolin-stimulated cAMP formation was inhibited by AEA and noladin ether (IC50: 69, 427 nM, respectively) to the same extent as by CP55.940 (Imax each approximately 30%) [8].
• Whereas noladin ether did not interact with AEA hydrolysis, this compound, 2-AG and virodhamine may share common enzymatic inactivation mechanisms in human neocortex [9].
• In addition, noladin ether caused a delay in wound healing of confluent trabecular meshwork monolayers and this effect of noladin ether was antagonized by SR141716A [10].

Anatomical context of Noladin

• Our results suggest, that AEA and noladin ether are full CB1 receptor agonists in human neocortex, whereas virodhamine may act as a CB1 receptor antagonist/inverse agonist [8].
• In the present study, we investigated the effects of noladin ether in the rat isolated mesenteric arterial bed, cultured dorsal root ganglia (DRG) cells and human vanilloid (TRPV1)-receptor-expressing HEK293 cells (TRPV1-HEK293 cells) [1].
• 7 These data demonstrate that noladin ether attenuates sensory neurotransmission in rat mesenteric arteries via a non-CB1 non-CB2 PTX-sensitive prejunctional site, independently of TRPV1 receptors [1].
• CONCLUSIONS: Noladin ether modulates the migration, adhesion, morphology, and actin cytoskeleton of TM cells [10].
• 2-Arachidonoyl glycerol and noladin ether (2-arachidonyl glyceryl ether), isolated in 1995 and 2001, respectively, so far, display pharmacological properties in the central nervous system, similar to those of anandamide [11].

Associations of Noladin with other chemical compounds

• Comparison of the enzymatic stability and intraocular pressure effects of 2-arachidonylglycerol and noladin ether, a novel putative endocannabinoid [12].
• 2-Eicosa-5',8',11',14'-tetraenylglycerol (2-AG ether, HU310, noladin ether) is a metabolically stable ether-linked analogue of 2-arachidonoylglycerol (2-AG), an endogenous cannabinoid receptor ligand [13].
• 4 Noladin ether had no effect on vasorelaxation elicited by exogenous CGRP or capsaicin [1].
• This study examined the ability of the endocannabinoids 2-arachidonoyl glycerol (2-AG) and noladin ether as well as the synthetic cannabinoid CP-55,940 [(-)-cis-3-[2-hydroxy-4-(1,1-dimethylheptyl)phenyl]-trans-4-(3-hydroxypropyl) cyclohexanol] to regulate three intracellular effectors via CB2 receptors in transfected Chinese hamster ovary cells [14].
• Anandamide (AEA), 2-arachidonyl glycerol (2-AG), 2-arachidonylglyceryl ether (noladin ether), O-arachidonyl ethanolamide (virodhamine), 2-linoleoyl glycerol (2-LG), arachidonyl glycine, oleoyl ethanolamide (OEA), and palmitoyl ethanolamide (PEA) were quantified by positive ion tandem electrospray ionization mass spectrometry [15].

Gene context of Noladin

• These data suggest that noladin ether is acting at a prejunctional site and no interaction with TRPV1 is involved [1].
• 2-AG and noladin ether require occupancy of less than one-half the number of receptors to produce comparable regulation of adenylyl cyclase and ERK-MAPK, relative to the synthetic cannabinoid CP-55,940 [14].
• When investigating survival of hippocampal neurons in culture, we found significant protection against hypoxia-induced cell death with CB1-analogs (noladin, (9-tetrahydrocannabinol) only in ETB-deficient neurons [16].
• 1 Noladin ether has recently been reported to be an endocannabinoid, with selectivity for the cannabinoid (CB) CB1 receptor [1].
• The endocannabinoid noladin ether acts as a full agonist at human CB2 cannabinoid receptors [17].

Analytical, diagnostic and therapeutic context of Noladin

• Noladin ether decreased IOP immediately after topical administration, and no initial IOP increase was observed in the treated eye [12].
• METHODS: The effects of noladin ether on aqueous humor outflow facility were measured in a porcine anterior-segment-perfused organ culture model [6].
• Both Western blot and zymography were used to monitor the effects of noladin ether on matrix metalloproteinase (MMP)-2 [6].

References