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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].
Medical cannabis and cannabinoids in rheumatology: where are we now?
Published in Expert Review of Clinical Immunology, 2019
Piercarlo Sarzi-Puttini, Alberto Batticciotto, Fabiola Atzeni, Laura Bazzichi, Manuela Di Franco, Fausto Salaffi, Daniela Marotto, Angela Ceribelli, Jacob N Ablin, Winfred Hauser
Trans-Δ9-tetrahydrocannabinol (THC, the primary psychoactive constituent of cannabis) was first isolated in the 1960s [6,7], and the identification of cannabinoid receptors 1 and 2 (CBr1 and CBr2) led to the isolation and characterization of their endogenous ligands, the endocannabinoids N-arachidonoyl-ethanolamine (AEA, also known as anandamide), 2-arachidonoylglycerol (2-AG), 2-archidonoylglyceral ether (noladin ether), O-archidonoyl ethanolamine (virodhamine) and N-arachidonoyl dopamine. Five main enzymes are involved in their biosynthesis and inactivation: N-acyl-phosphatidylethanolamine-hydrolyzing phospholipase D (NAPE-PLD), sn-1-specific diacylglycerol lipase-α (DGLα), DGLβ, fatty acid amide hydrolase 1 (FAAH), and monoacylglycerol lipase (MAGL, also known as MGL) [8–10].
Cannabinoid hyperemesis syndrome: potential mechanisms for the benefit of capsaicin and hot water hydrotherapy in treatment
Published in Clinical Toxicology, 2018
John R. Richards, Jeff M. Lapoint, Guillermo Burillo-Putze
The TRPV1 receptor is an outwardly rectifying, nonselective cation channel located on C and Aδ peripheral nociceptive neurons and in the brain, gastrointestinal tract, airways, bladder, and kidney [25]. Capsaicin binding activates the TRPV1 receptor triggering influx of calcium and sodium, as well as release of inflammatory neuropeptides leading to transient burning, stinging, and itching [39]. TRPV1 receptors are also expressed on the endoplasmic reticulum and regulate intracellular calcium concentrations [40]. In addition to TRPV1, capsaicin-sensitive receptors express several other members of the transient receptor potential channel family. These receptors respond to noxious stimuli, such as heat (>43 °C), acids (pH <6), pain, and change in osmolarity, as well as endogenous lipid compounds, termed endovanilloids [41]. The endovanilloids, which include anandamide and N-arachidonoyl-dopamine, induce TRPV1 currents much smaller than those evoked by topical capsaicin [42]. The action of topical capsaicin may mimic the effect of heat-activation of TRPV1.