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Recent Cannabinoid Delivery Systems
Published in Betty Wedman-St Louis, Cannabis as Medicine, 2019
Natascia Bruni, Carlo Della Pepa, Simonetta Oliaro-Bosso, Daniela Gastaldi, Franco Dosio, Enrica Pessione
Overall, seven different endogenous ligands have been identified as acting within the endocannabinoid system to date. The first two endocannabinoids are the derivatives of arachidonic acid N-arachidonoyl ethanolamide (anandamide) and 2-arachidonoylglycerol [12]. A third endocannabinoid, 2-arachidonoyl glyceryl ether (noladin ether), was discovered in 2001. N-arachidonoyl dopamine, O-arachidonoyl-ethanolamide (virodhamine), docosatetraenoylethanolamide, lysophosphatidylinositol, and oleoylethanolamide have since been described as ligands of endocannabinoid receptors [7].
The Relaxation System Theoretical Construct
Published in Len Wisneski, The Scientific Basis of Integrative Health, 2017
As of this writing, there are five known endogenous ligands for the cannabinoid receptor. They are referred to as endocannabinoids, as they are endogenous cannabinoids. First, anandamide, as stated, was discovered in 1992. Next, in 1995, 2-AG was identified simultaneously by Mechoulam's group in Israel and by a group in Japan led by Takayuki Sugiura. Then, the endogenous ligand, 2-arachidonoyl-glycerol ether, which the researchers call noladin ether, was located through the efforts of Mechoulam and colleagues in Israel (Devane et al., 1992; Hanus et al., 2001; Mechoulam et al., 1995; Sugiura et al., 1995). Finally and most recently, virodhamine and N-arachidonoyldopamine have been located, but very little has been published on either of them (Chu et al., 2003; Porter et al., 2002; Walker et al., 2002). Parenthetically, there are also numerous synthetic agonists and novel analogs that have been developed for research purposes (Hanus et al., 1999; Priller et al., 1995; Suhara et al., 2001). We will not cover these agonists, as our work is directed toward understanding the hormones involved in the theta healing system.
Medical marijuana for inflammatory bowel disease: the highs and lows
Published in Scandinavian Journal of Gastroenterology, 2022
The endocannabinoid system is composed primarily of the G protein coupled cannabinoid receptors CB1 and CB2 (also known as CNR1 and CNR2 respectively); endogenous cannabinoids targeting these and other receptors; and enzymes catalyzing the biosynthesis and metabolism of endocannabinoids [13]. Other cannabinoid receptors include transient receptor potential vanilloid type 1 (TRPV1), peroxisome proliferator activated receptor-α, and orphan G protein coupled receptors GPR55 and GPR119 [15], but this review article will be focusing on the CB1 and CB2 receptors. The two endocannabinoids that have been most studied are N-arachidonoylethanolamine (anandamine) and 2-arachidonoylglycerol (2-AG), both of which exert most of their functions by binding to and activating CB1 and CB2 receptors [16]. CB1 receptors are found predominantly at central and peripheral nerve terminals and mediate the inhibition of neurotransmitter release. CB2 receptors are found mainly on immune cells and one of their key roles appears to be in the modulation of cytokine release [17]. Atypical endocannabinoids include 2-arachidonoylglycerol ether (noladin ether), N-arachidonoyl dopamine (NADA), virodhamine, N-homo-γ-linolenoyl-ethanolamine (HEA), N-docosatetraenoyl-ethanolamine (DEA), palmitoylethanolamide (PEA), and oleoylethanolamide; these endocannabinoids bind to non CB1 and CB2 receptors and their roles in the endocannabinoid system are less clearly defined [18].
Targeting the endocannabinoid system as a potential anticancer approach
Published in Drug Metabolism Reviews, 2018
Rico Schwarz, Robert Ramer, Burkhard Hinz
Virodhamine, an ester derivative of arachidonic acid (AA) and ethanolamine, was shown to act as CB1 receptor antagonist and CB2 receptor agonist (Porter et al. 2002). A non-enzymatic transformation of N-acylethanolamines into the corresponding O-acyl esters and vice versa was reported to be catalyzed by bases as well as acids (Markey et al. 2000). De Petrocellis et al. (2004) have suggested a switch from CB1- to CB2-mediated responses and vice versa by the conversion of AEA into virodhamine, and by virodhamine into AEA, respectively. In a further investigation, virodhamine has been shown to inhibit the activity of FAAH in a concentration-dependent manner (Steffens et al. 2005). The authors of this study further suggested that, similar to 2-AG, virodhamine serves as substrate hydrolyzed by MAGL. Later Brantl et al. (2014) provided evidence for 2-AG and virodhamine as probable enzymatic substrates of MAGL. In fact, both endocannabinoids were demonstrated to elicit platelet activation which resembled AA-induced aggregation and was blocked by the cyclooxygenase-1 (COX-1) inhibitor acetylsalicylic acid and by a thromboxane A2 receptor antagonist accordingly. Moreover, platelet activation by 2-AG and virodhamine was inhibited by the MAGL inhibitor JZL184, suggesting both endocannabinoids to stimulate platelets via a MAGL-triggered mechanism leading to free AA and its COX-1-dependent metabolism to proaggretory thromboxane A2 (Brantl et al. 2014). Finally, AEA, 2-AG, NADA, noladin ether, and virodhamine have been identified as GPR55 agonists (Ryberg et al. 2007; Akimov et al. 2017).