Sierra Acai Company
Sierra Acai Company
Open 7 Days a Week
MonaVie Independent Distributor
Distributor Training
Shop Online
Enroll Now
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
Friends
Buy Wholesale and maintain an Active status for 2 months and we will refund your $39 Distributor Fee
11-SEPTEMBER-2008 12:20:15 - Cannabinoids Redirected from Endocannabinoid Cannabinoids pronounced /kəˈnæbɨˌnɔɪdz/1 are a group of terpenophenolic compounds present in Cannabis Cannabis sativa L. The broader definition of cannabinoids refer to a group of substances that are structurally related to tetrahydrocannabinol THC or that bind to cannabinoid receptors. The chemical definition encompasses a variety of distinct chemical classes: the classical cannabinoids structurally related to THC, the nonclassical cannabinoids, the aminoalkylindoles, the eicosanoids related to the endocannabinoids, 1,5-diarylpyrazoles, quinolines and arylsulphonamides and additional compounds that do not fall into these standard classes but bind to cannabinoid receptors.2 The term cannabinoids also refers to a unique group of secondary metabolites found in the cannabis plant, which are responsible for the plant's peculiar pharmacological effects. Currently, there are three general types of cannabinoids: phytocannabinoids occur uniquely in the cannabis plant; endogenous cannabinoids are produced in the bodies of humans and other animals; and synthetic cannabinoids are similar compounds produced in a laboratory. Contents 1 Cannabinoid receptors 2 Phytocannabinoids 2.1 Types 2.1.1 Tetrahydrocannabinol 2.1.2 Cannabidiol 2.1.3 Cannabinol 2.1.4 Tetrahydrocannabivarin 2.1.5 Cannabichromene 2.1.6 Double bond position 2.1.7 Length 2.1.8 Plant profile 2.2 Pharmacology 2.3 Production 2.3.1 Plant synthesis 2.3.2 Separation 2.4 History 3 Endocannabinoids 3.1 Types of endocannabinoid ligands 3.2 Function 3.2.1 Retrograde signal 3.2.2 Range 3.3 Other thoughts 3.4 U.S. Patent # 6630507 4 Synthetic and patented cannabinoids 5 Table of natural cannabinoids 6 References 7 Notes 8 External links Cannabinoid receptors Main article: cannabinoid receptor Before the 1980s, it was often speculated that cannabinoids produced their physiological and behavioral effects via nonspecific interaction with cell membranes, instead of interacting with specific membrane-bound receptors. The discovery of the first cannabinoid receptors in the 1980s helped to resolve this debate. These receptors are common in animals, and have been found in mammals, birds, fish, and reptiles. There are currently two known types of cannabinoid receptors, termed CB1 and CB2. CB1 receptors are found primarily in the brain, specifically in the basal ganglia and in the limbic system, including the hippocampus. They are also found in the cerebellum and in both male and female reproductive systems. CB1 receptors are essentially absent in the medulla oblongata, the part of the brain stem that is responsible for respiratory and cardiovascular functions. Thus, there is not a risk of respiratory or cardiovascular failure as there is with many other drugs. CB1 receptors appear to be responsible for the euphoric and anticonvulsive effects of cannabis. CB2 receptors are almost exclusively found in the immune system, with the greatest density in the spleen. While generally found only in the peripheral nervous system, a report does indicate that CB2 is expressed by a subpopulation of microglia in the human cerebellum 3. CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis. Phytocannabinoids Type Skeleton Cyclization Cannabigerol-type CBG Chemical structure of a CBG-type cannabinoid. Chemical structure of the CBG-type cyclization of cannabinoids. Cannabichromene-type CBC Chemical structure of a CBC-type cannabinoid. Chemical structure of the CBC-type cyclization of cannabinoids. Cannabidiol-type CBD Chemical structure of a CBD-type cannabinoid. Chemical structure of the CBD-type cyclization of cannabinoids. Tetrahydrocannabinol- and Cannabinol-type THC, CBN Chemical structure of a CBN-type cannabinoid. Chemical structure of the CBN-type cyclization of cannabinoids. Cannabielsoin-type CBE Chemical structure of a CBE-type cannabinoid. Chemical structure of the CBE-type cyclization of cannabinoids. iso- Tetrahydrocannabinol- type iso-THC Chemical structure of an iso-CBN-type cannabinoid. Chemical structure of the iso-CBN-type cyclization of cannabinoids. Cannabicyclol-type CBL Chemical structure of a CBL-type cannabinoid. Chemical structure of the CBL-type cyclization of cannabinoids. Cannabicitran-type CBT Chemical structure of a CBT-type cannabinoid. Chemical structure of the CBT-type cyclization of cannabinoids. Main classes of natural cannabinoids Phytocannabinoids, also called natural cannabinoids, herbal cannabinoids, and classical cannabinoids, are only known to occur naturally in significant quantity in the cannabis plant, and are concentrated in a viscous resin that is produced in glandular structures known as trichomes. In addition to cannabinoids, the resin is rich in terpenes, which are largely responsible for the odour of the cannabis plant. Phytocannabinoids are nearly insoluble in water but are soluble in lipids, alcohols, and other non-polar organic solvents. However, as phenols they form more water-soluble phenolate salts under strongly alkaline conditions. All natural cannabinoids are derived from their respective 2-carboxylic acids 2-COOH by decarboxylation catalyzed by heat, light, or alkaline conditions. Types At least 66 cannabinoids have been isolated from the cannabis plant4 To the right the main classes of natural cannabinoids are shown. All classes derive from cannabigerol-type compounds and differ mainly in the way this precursor is cyclized. Tetrahydrocannabinol THC, cannabidiol CBD and cannabinol CBN are the most prevalent natural cannabinoids and have received the most study. Other common cannabinoids are listed below: CBG Cannabigerol CBC Cannabichromene CBL Cannabicyclol CBV Cannabivarin THCV Tetrahydrocannabivarin CBDV Cannabidivarin CBCV Cannabichromevarin CBGV Cannabigerovarin CBGM Cannabigerol Monoethyl Ether Tetrahydrocannabinol Main article: Tetrahydrocannabinol Tetrahydrocannabinol THC is the primary psychoactive component of the plant. Medically, it appears to ease moderate pain analgetic and to be neuroprotective. THC has approximately equal affinity for the CB1 and CB2 receptors.5 Its effects are perceived to be more cerebral.citation needed delta-9-Tetrahydrocannabinol Δ9-THC, THC and delta-8-tetrahydrocannabinol Δ8-THC, mimic the action of anandamide, a neurotransmitter produced naturally in the body. The THCs produce the high associated with cannabis by binding to the CB1 cannabinoid receptors in the brain. Cannabidiol Main article: cannabidiol Cannabidiol CBD is not psychoactive, and was thought to not affect the psychoactivity of THC6. However, recent evidence shows that smokers of cannabis with a high CBD/THC ratio were less likely to experience THC-induced psychosis.citation needed This is supported by psychological tests, in which participants experience less intense psychotic effects when intravenous THC was coadministered with CBD as measured with a PANSS test. 7. It has been hypothesised that CBD acts as an allosteric antagonist at the CB1 receptor and thus alters the psychoactive effects of THC.citation needed Medically, it appears to relieve convulsion, inflammation, anxiety, and nausea.citation needed CBD has a greater affinity for the CB2 receptor than for the CB1 receptor. It is perceived to have more effect on the body.citation needed CBD shares a precursor with THC and is the main cannabinoid in low-THC Cannabis strains. Cannabinol Main article: cannabinol Cannabinol CBN is the primary product of THC degradation, and there is usually little of it in a fresh plant. CBN content increases as THC degrades in storage, and with exposure to light and air. It is only mildly psychoactive. Tetrahydrocannabivarin Main article: Tetrahydrocannabivarin Tetrahydrocannabivarin THCV is prevalent in certain South African and Southeast Asian strains of Cannabis. It is an antagonist of THC at CB1 receptors and attenuates the psychoactive effects of THC.8 Cannabichromene Main article: Cannabichromene Cannabichromene CBC is non-psychoactive and does not affect the psychoactivity of THC 6. Double bond position In addition, each of the compounds above may be in different forms depending on the position of the double bond in the alicyclic carbon ring. There is potential for confusion because there are different numbering systems used to describe the position of this double bond. Under the dibenzopyran numbering system widely used today, the major form of THC is called delta-9-THC, while the minor form is called delta-8-THC. Under the alternate terpene numbering system, these same compounds are called delta-1-THC and delta-6-THC, respectively. Length Most herbal cannabinoid compounds are 21 carbon compounds. However, some do not follow this rule, primarily because of variation in the length of the side chain attached to the aromatic ring. In THC, CBD, and CBN, this side chain is a pentyl 5 carbon chain. In the most common homologue, the pentyl chain is replaced with a propyl 3 carbon chain. Cannabinoids with the propyl side chain are named using the suffix varin, and are designated, for example, THCV, CBDV, or CBNV. It appears that shorter chains increase the intensity and decrease the duration of the activity of the chemicals. Plant profile Cannabis plants can exhibit wide variation in the quantity and type of cannabinoids they produce. The mixture of cannabinoids produced by a plant is known as the plant's cannabinoid profile. Selective breeding has been used to control the genetics of plants and modify the cannabinoid profile. For example, strains which are used as fiber commonly called hemp, are bred such that they are low in psychoactive chemicals like THC. Strains used in medicine are often bred for high CBD content, and strains used for recreational purposes are usually bred for high THC content, or for a specific chemical balance. Some strains of more than 20% THC in their flowering buds have been created.citation needed Quantitative analysis of a plant's cannabinoid profile is usually determined by gas chromatography GC, or more reliably by gas chromatography combined with mass spectrometry GC/MS. Liquid chromatography LC techniques are also possible, although these are often only semi-quantitative or qualitative. There have been systematic attempts to monitor the cannabinoid profile of cannabis over time, but their accuracy is impeded by the illegal status of the plant in many countries. Pharmacology Cannabinoids can be administered by smoking, vaporizing, oral ingestion, transdermal patch, intravenous injection, sublingual absorption, or rectal suppository. Once in the body, most cannabinoids are metabolized in the liver, especially by cytochrome P450 mixed-function oxidases, mainly CYP 2C9. Thus supplementing with CYP 2C9 inhibitors leads to extended intoxication. Some is also stored in fat in addition to being metabolized in liver. Delta-9-THC is metabolized to 11-hydroxy-delta-9-THC, which is then metabolized to 9-carboxy-THC. Some cannabis metabolites can be detected in the body after several weeks. Production Production of cannabinoids include both the synthesis in the plant, and separation of certain types from this material. Plant synthesis Cannabinoid production starts when an enzyme causes geranyl pyrophosphate and olivetolic acid to combine and form CBG. Next, CBG is independently converted to either CBD or CBC by two separate synthase enzymes. CBC is then enzymatically cyclized to THC. For the propyl homologues THCV, CBDV and CBNV, there is a similar pathway that is based on CBGV. Separation Cannabinoids can be separated from the plant by extraction with organic solvents. Hydrocarbons and alcohols are often used as solvents. However, these solvents are flammable and many are toxic. Supercritical solvent extraction with carbon dioxide is an alternative technique. Although this process requires high pressures, there is minimal risk of fire or toxicity, solvent removal is simple and efficient, and extract quality can be well-controlled. Once extracted, cannabinoid blends can be separated into individual components using wiped film vacuum distillation or other distillation techniques. However, to produce high purity cannabinoids, chemical synthesis or semisynthesis is generally required. History Cannabinoids were first discovered in the 1940s, when CBD and CBN were identified. The structure of THC was first determined in 1964. Due to molecular similarity and ease of synthetic conversion, it was originally believed that CBD was a natural precursor to THC. However, it is now known that CBD and THC are produced independently in the cannabis plant. Endocannabinoids For more details on the roles and regulation of the endocannabinoids, see Endocannabinoid system. Anandamide, an endogenous ligand of CB1 and CB2 Anandamide, an endogenous ligand of CB1 and CB2 Endocannabinoids are substances produced from within the body which activate cannabinoid receptors. After the discovery of the first cannabinoid receptor in 1988, scientists began searching for an endogenous ligand for the receptor. Types of endocannabinoid ligands Arachidonoyl ethanolamide Anandamide or AEA In 1992, the first such compound was identified as arachidonoyl ethanolamide and named anandamide, a name derived from the Sanskrit word for bliss and -amide. Anandamide is derived from the essential fatty acid arachidonic acid. It has a pharmacology similar to THC, although its chemical structure is different. Anandamide binds to the central CB1 and, to a lesser extent, peripheral CB2 cannabinoid receptors, where it acts as a partial agonist. Anandamide is about as potent as THC at the CB1 receptor.9 It is found in nearly all tissues in a wide range of animals.citation needed Two analogs of anandamide, 7,10,13,16-docosatetraenoylethanolamide and homo-γ-linolenoylethanolamide, have similar pharmacology. All of these are members of a family of signalling lipids called N-acylethanolamides, which also includes the noncannabimimetic palmitoylethanolamide and oleoylethanolamide which possess anti-inflammatory and orexigenic effects, respectively. Many N-acylethanolamides have also been identified in plant seeds10 and in molluscs.11 2-arachidonoyl glycerol 2-AG Another endocannabinoid, 2-arachidonoyl glycerol, binds to both the CB1 and CB2 receptors with similar affinity, acting as a full agonist at both.9 2-AG is present at significantly higher concentrations in the brain than anandamide12, and there is some controversy over whether 2-AG rather than anandamide is chiefly responsible for endocannabinoid signalling in vivo13. In particular, one in vitro study suggests that 2-AG is capable of stimulating higher G-protein activation than anandamide, although the physiological implications of this finding are not yet known.14 2-arachidonyl glyceryl ether noladin ether In 2001 a third, ether-type endocannabinoid, 2-arachidonyl glyceryl ether noladin ether, was isolated from porcine brain. 15 Prior to this discovery, it had been synthesized as a stable analog of 2-AG; indeed, some controversy remains over its classification as an endocannabinoid, as another group failed to detect the substance at any appreciable amount in the brains of several different mammalian species.16 It binds to the CB1 cannabinoid receptor Ki = 21.2 nmol/L and causes sedation, hypothermia, intestinal immobility, and mild antinociception in mice. It binds primarily to the CB1 receptor, and only weakly to the CB2 receptor.9 N-arachidonoyl-dopamine NADA Discovered in 2000, NADA preferentially binds to the CB1 receptor.17 Like anandamide, NADA is also an agonist for the vanilloid receptor subtype 1 TRPV1, a member of the vanilloid receptor family.1819 Virodhamine OAE A fifth endocannabinoid, virodhamine, or O-arachidonoyl-ethanolamine OAE was discovered in June 2002. Although it is a full agonist at CB2 and a partial agonist at CB1, it behaves as a CB1 antagonist in vivo. In rats, virodhamine was found to be present at comparable or slightly lower concentrations than anandamide in the brain, but 2- to 9-fold higher concentrations peripherally.20 Function Endocannabinoids serve as intercellular 'lipid messengers', signaling molecules that are released from one cell and activate the cannabinoid receptors present on other nearby cells. Although in this intercellular signaling role they are similar to the well-known monoamine neurotransmitters, such as acetylcholine, GABA or dopamine, endocannabinoids differ in numerous ways from them. For instance, they use retrograde signaling. Furthermore, endocannabinoids are lipophilic molecules that are not very soluble in water. They are not stored in vesicles, and exist as integral constituents of the membrane bilayers that make up cells. They are believed to be synthesized 'on-demand' rather than made and stored for later use. The mechanisms and enzymes underlying the biosynthesis of endocannabinoids remain elusive and continue to be an area of active research. The endocannabinoid 2-AG has been found in bovine and human maternal milk.21 Retrograde signal Conventional neurotransmitters are released from a 'presynaptic' cell and activate appropriate receptors on a 'postsynaptic' cell, where presynaptic and postsynaptic designate the sending and receiving sides of a synapse, respectively. Endocannabinoids, on the other hand, are described as retrograde transmitters because they most commonly travel 'backwards' against the usual synaptic transmitter flow. They are in effect released from the postsynaptic cell and act on the presynaptic cell, where the target receptors are densely concentrated on axonal terminals in the zones from which conventional neurotransmitters are released. Activation of cannabinoid receptors temporarily reduces the amount of conventional neurotransmitter released. This endocannabinoid mediated system permits the postsynaptic cell to control its own incoming synaptic traffic. The ultimate effect on the endocannabinoid releasing cell depends on the nature of the conventional transmitter that is being controlled. For instance, when the release of the inhibitory transmitter, GABA, is reduced, the net effect is an increase in the excitability of the endocannabinoid-releasing cell. Conversely, when release of the excitatory neurotransmitter, glutamate, is reduced, the net effect is a decrease in the excitability of the endocannabinoid-releasing cell. Range Endocannabinoids are hydrophobic molecules. They cannot travel unaided for long distances in the aqueous medium surrounding the cells from which they are released, and therefore act locally on nearby target cells. Hence, although emanating diffusely from their source cells, they have much more restricted spheres of influence than do hormones, which can affect cells throughout the body. Other thoughts Endocannabinoids constitute a versatile system for affecting neuronal network properties in the nervous system. Scientific American published an article in December 2004, entitled The Brain's Own Marijuana discussing the endogenous cannabinoid system. 22 The current understanding recognizes the role that endocannabinoids play in almost every major life function in the human body.citation needed Cannabinoids act as a bioregulatory mechanism for most life processes, which reveals why medical cannabis has been cited as treatments for many diseases and ailments in anecdotal reports and scientific literature. Some of these ailments include: pain, arthritic conditions, migraine headaches, anxiety, epileptic seizures, insomnia, loss of appetite, GERD chronic heartburn, nausea, glaucoma, AIDS wasting syndrome, depression, bipolar disorder particularly depression-manic-normal, multiple sclerosis, menstrual cramps, Parkinson's, trigeminal neuralgia tic douloureux, high blood pressure, irritable bowel syndrome, and bladder incontinence. U.S. Patent # 6630507 In 2003, the U.S. Government as represented by the Department of Health and Human Services filed for, and was awarded a patent on cannabinoids as antioxidants and neuroprotectants. U.S. Patent 6630507. Synthetic and patented cannabinoids Historically, laboratory synthesis of cannabinoids were often based on the structure of herbal cannabinoids and a large number of analogs have been produced and tested, especially in a group led by Roger Adams as early as 1941 and later in a group led by Raphael Mechoulam. Newer compounds are no longer related to natural cannabinoids or are based on the structure of the endogenous cannabinoids. Synthetic cannabinoids are particularly useful in experiments to determine the relationship between the structure and activity of cannabinoid compounds, by making systematic, incremental modifications of cannabinoid molecules. Medications containing natural or synthetic cannabinoids or cannabinoid analogs: Dronabinol Marinol, is Δ9-tetrahydrocannabinol THC, used as an appetite stimulant, anti-emetic and analgesic. Nabilone Cesamet, a synthetic cannabinoid and an analog of Marinol. It is Schedule II unlike Marinol which is Schedule III. Sativex, a cannabinoid extract oral spray containing THC, CBD, and other cannabinoids used for neuropathic pain and spasticity in Canada and Spain. Sativex develops whole plant cannabinoid medicines. Rimonabant SR141716, a selective cannabinoid CB1 receptor antagonist used as an anti-obesity drug under the proprietary name, Acomplia. It is also used for smoking cessation. Other notable synthetic cannabinoids include: CP-55940, produced in 1974, this synthetic cannabinoid receptor agonist is many times more potent than THC Dimethylheptylpyran HU-210, about 100 times as potent as THC23. SR144528, a CB2 receptor antagonists WIN 55,212-2, a potent cannabinoid receptor agonist JWH-133, a potent selective CB2 receptor agonist. Levonantradol Nantrodolum, an anti-emetic and analgesic but not currently in use in medicine. Table of natural cannabinoids Cannabigerol-type CBG Chemical structure of cannabigerol. Cannabigerol E-CBG-C5 Chemical structure of cannabigerol monomethyl ether. Cannabigerol monomethyl ether E-CBGM-C5 A Chemical structure of cannabinerolic acid A. Cannabinerolic acid A Z-CBGA-C5 A Chemical structure of cannabigerovarin. Cannabigerovarin E-CBGV-C3 Chemical structure of cannabigerolic acid A. Cannabigerolic acid A E-CBGA-C5 A Chemical structure of cannabigerolic acid A monomethyl ether. Cannabigerolic acid A monomethyl ether E-CBGAM-C5 A Chemical structure of cannabigerovarinic acid A. Cannabigerovarinic acid A E-CBGVA-C3 A Cannabichromene-type CBC Chemical structure of cannabichromene. ±-Cannabichromene CBC-C5 Chemical structure of cannabichromenic acid A. ±-Cannabichromenic acid A CBCA-C5 A Chemical structure of cannabichromevarine. ±-Cannabivarichromene, ±-Cannabichromevarin CBCV-C3 Chemical structure of cannabichromevarinic acid A. ±-Cannabichromevarinic acid A CBCVA-C3 A Cannabidiol-type CBD Chemical structure of cannabidiol. --Cannabidiol CBD-C5 Chemical structure of cannabidiol momomethyl ether. Cannabidiol momomethyl ether CBDM-C5 Chemical structure of cannabidiol-C4 Cannabidiol-C4 CBD-C4 Chemical structure of cannabidivarin. --Cannabidivarin CBDV-C3 Chemical structure of cannabidiorcol. Cannabidiorcol CBD-C1 Chemical structure of cannabidiolic acid. Cannabidiolic acid CBDA-C5 Chemical structure of cannabidivarinic acid. Cannabidivarinic acid CBDVA-C3 Cannabinodiol-type CBND Chemical structure of cannabinodiol. Cannabinodiol CBND-C5 Chemical structure of cannabinodivarin. Cannabinodivarin CBND-C3 Tetrahydrocannabinol-type THC Chemical structure of delta-9-tetrahydrocannabinol. Δ9-Tetrahydrocannabinol Δ9-THC-C5 Chemical structure of delta-9-tetrahydrocannabinol-C4 Δ9-Tetrahydrocannabinol-C4 Δ9-THC-C4 Chemical structure of delta-9-tetrahydrocannabivarin. Δ9-Tetrahydrocannabivarin Δ9-THCV-C3 Chemical structure of tetrahydrocannabiorcol. Δ9-Tetrahydrocannabiorcol Δ9-THCO-C1 Chemical structure of delta-9-tetrahydrocannabinolic acid A. Δ9-Tetrahydro- cannabinolic acid A Δ9-THCA-C5 A Chemical structure of delta-9-tetrahydrocannabinolic acid B. Δ9-Tetrahydro- cannabinolic acid B Δ9-THCA-C5 B Chemical structure of delta-9-tetrahydrocannabinolic acid-C4 Δ9-Tetrahydro- cannabinolic acid-C4 A and/or B Δ9-THCA-C4 A and/or B Chemical structure of delta-9-tetrahydrocannabivarinic acid A. Δ9-Tetrahydro- cannabivarinic acid A Δ9-THCVA-C3 A Chemical structure of delta-9-tetrahydrocannabiorcolic acid. Δ9-Tetrahydro- cannabiorcolic acid A and/or B Δ9-THCOA-C1 An and/or B Chemical structure of delta-8-tetrahydrocannabinol. --Δ8-trans-6aR,10aR- Δ8-Tetrahydrocannabinol Δ8-THC-C5 Chemical structure of delta-8-tetrahydrocannabinolic acid A. --Δ8-trans-6aR,10aR- Tetrahydrocannabinolic acid A Δ8-THCA-C5 A Chemical structure of cis-delta-9-tetrahydrocannabinol. --6aS,10aR-Δ9- Tetrahydrocannabinol --cis-Δ9-THC-C5 Cannabinol-type CBN Chemical structure of cannabinol. Cannabinol CBN-C5 Chemical structure of cannabinol-C4 Cannabinol-C4 CBN-C4 Chemical structure of cannabivarin. Cannabivarin CBN-C3 Chemical structure of cannabinol-C2 Cannabinol-C2 CBN-C2 Chemical structure of cannabiorcol. Cannabiorcol CBN-C1 Chemical structure of cannabinolic acid A. Cannabinolic acid A CBNA-C5 A Chemical structure of cannabinol methyl ether. Cannabinol methyl ether CBNM-C5 Cannabitriol-type CBT Chemical structure of --trans-cannabitriol. --9R,10R-trans- Cannabitriol --trans-CBT-C5 Chemical structure of +-trans-cannabitriol. +-9S,10S-Cannabitriol +-trans-CBT-C5 Chemical structure of cis-cannabitriol. ±-9R,10S/9S,10R- Cannabitriol ±-cis-CBT-C5 Chemical structure of trans-cannabitriol ethyl ether. --9R,10R-trans- 10-O-Ethyl-cannabitriol --trans-CBT-OEt-C5 Chemical structure of trans-cannabitriol-C3 ±-9R,10R/9S,10S- Cannabitriol-C3 ±-trans-CBT-C3 Chemical structure of 8,9-dihydroxy-delta-6a10a-tetrahydrocannabinol. 8,9-Dihydroxy-Δ6a10a- tetrahydrocannabinol 8,9-Di-OH-CBT-C5 Chemical structure of cannabidiolic acid A cannabitriol ester. Cannabidiolic acid A cannabitriol ester CBDA-C5 9-OH-CBT-C5 ester Chemical structure of cannabiripsol. --6aR,9S,10S,10aR- 9,10-Dihydroxy- hexahydrocannabinol, Cannabiripsol Cannabiripsol-C5 Chemical structure of cannabitetrol. --6a,7,10a-Trihydroxy- Δ9-tetrahydrocannabinol --Cannabitetrol Chemical structure of 10-oxo-delta-6a10a-tetrahydrocannabinol. 10-Oxo-Δ6a10a- tetrahydrocannabinol OTHC Cannabielsoin-type CBE Chemical structure of cannabielsoin. 5aS,6S,9R,9aR- Cannabielsoin CBE-C5 Chemical structure of C3-cannabielsoin. 5aS,6S,9R,9aR- C3-Cannabielsoin CBE-C3 Chemical structure of cannabielsoic acid A. 5aS,6S,9R,9aR- Cannabielsoic acid A CBEA-C5 A Chemical structure of cannabielsoic acid B. 5aS,6S,9R,9aR- Cannabielsoic acid B CBEA-C5 B Chemical structure of C3-cannabielsoic acid B. 5aS,6S,9R,9aR- C3-Cannabielsoic acid B CBEA-C3 B Chemical structure of cannabiglendol-C3 Cannabiglendol-C3 OH-iso-HHCV-C3 Chemical structure of dehydrocannabifuran. Dehydrocannabifuran DCBF-C5 Chemical structure of cannabifuran. Cannabifuran CBF-C5 Isocannabinoids Chemical structure of delta-7-trans-isotetrahydrocannabinol. --Δ7-trans-1R,3R,6R- Isotetrahydrocannabinol Chemical structure of delta-7-cis-isotetrahydrocannabivarin. ±-Δ7-1,2-cis- 1R,3R,6S/1S,3S,6R- Isotetrahydro- cannabivarin Chemical structure of delta-7-trans-isotetrahydrocannabivarin. --Δ7-trans-1R,3R,6R- Isotetrahydrocannabivarin Cannabicyclol-type CBL Chemical structure of cannabicyclol. ±-1aS,3aR,8bR,8cR- Cannabicyclol CBL-C5 Chemical structure of cannabicyclolic acid A. ±-1aS,3aR,8bR,8cR- Cannabicyclolic acid A CBLA-C5 A Chemical structure of cannabicyclovarin. ±-1aS,3aR,8bR,8cR- Cannabicyclovarin CBLV-C3 Cannabicitran-type CBT Chemical structure of cannabicitran. Cannabicitran CBT-C5 Cannabichromanone-type CBCN Chemical structure of cannabichromanone. Cannabichromanone CBCN-C5 Chemical structure of cannabichromanone-C3 Cannabichromanone-C3 CBCN-C3 Chemical structure of cannabicoumaronone. Cannabicoumaronone CBCON-C5 References ^ 2000 The American Heritage Dictionary, 4th ed., Houghton Mifflin. ISBN 0395825172. ^ Lambert DM, Fowler CJ 2005. The endocannabinoid system: drug targets, lead compounds, and potential therapeutic applications. J. Med. Chem. 48 16: 5059-87. doi:10.1021/jm058183t. PMID 16078824. ^ Núñez E, Benito C, Pazos MR, et al 2004. Cannabinoid CB2 receptors are expressed by perivascular microglial cells in the human brain: an immunohistochemical study. Synapse 53 4: 208-13. doi:10.1002/syn.20050. PMID 15266552. ^ Burns TL, Ineck JR. Cannabinoid analgesia as a potential new therapeutic option in the treatment of chronic pain. The Annals of Pharmacotherapy. 2006 Feb;402:251-60. PMID 16449552 ^ Huffman JW 2000. The search for selective ligands for the CB2 receptor. Curr. Pharm. Des. 6 13: 1323-37. doi:10.2174/1381612003399347. PMID 10903395. ^ a b Behavioural Pharmacology - Abstract: Volume 165-6 September 2005 p 487-496 Neurophysiological and subjective profile of marijuana with varying concentrations of cannabinoids.. Retrieved on 2007-06-24. ^ Should I Smoke Dope?. Retrieved on 2008-05-24. ^ British Journal of Pharmacology - Abstract of article: Evidence that the plant cannabinoid delta-9-tetrahydrocannabivarin is a cannabinoid CB1 and CB2 receptor antagonist. Retrieved on 2007-06-24. ^ a b c Grotenhermen F. Cannabinoids. Current Drug Targets - CNS Neurological Disorders. 2005 Oct;45:507-30. PMID 16266285 ^ N-Acylethanolamines in Seeds. Quantification of Molecular Species and Their Degradation upon Imbibition -- Chapman et al. 120 4: 1157 -- PLANT PHYSIOLOGY. Retrieved on 2007-06-24. ^ ScienceDirect - Biochimica et Biophysica Acta BBA - Lipids and Lipid Metabolism : Bioactive long chain N-acylethanolamines in five species of edible bivalve molluscs: Possible implications for mollusc physiology and sea food industry. doi:10.1016/S0005-27609700132-X. Retrieved on 2007-06-24. ^ Stella N, Schweitzer P, Piomelli D. A second endogenous cannabinoid that modulates long-term potentiation. Nature. 1997 Aug 21; 3886644:773-8. PMID 9285589 ^ reviewed in Pacher P, Batkai S, Kunos G. The endocannabinoid system as an emerging target of pharmacotherapy. Pharmacological Reviews. 2006 Sep;583:389-462. PMID 16968947 ^ Savinainen JR, Jarvinen T, Laine K, Laitinen JT. Despite substantial degradation, 2-arachidonoylglycerol is a potent full efficacy agonist mediating CB1 receptor-dependent G-protein activation in rat cerebellar membranes. British Journal of Pharmacology. 2001 Oct; 1343:664-72. PMID 11588122 ^ Hanus L, Abu-Lafi S, Fride E, et al 2001. 2-arachidonyl glyceryl ether, an endogenous agonist of the cannabinoid CB1 receptor. Proc. Natl. Acad. Sci. U.S.A. 98 7: 3662-5. doi:10.1073/pnas.061029898. PMID 11259648. ^ Oka S, Tsuchie A, Tokumura A, Muramatsu M, Suhara Y, Takayama H, Waku K, Sugiura T. Ether-linked analogue of 2-arachidonoylglycerol noladin ether was not detected in the brains of various mammalian species. Journal of Neurochemistry. 2003 Jun;856:1374-81. PMID 12787057 ^ Bisogno, T., D. Melck, M. Bobrov, N. M. Gretskaya, V. V. Bezuglov, L. De Petrocellis, V. Di Marzo. N-acyl-dopamines: novel synthetic CB1 cannabinoid-receptor ligands and inhibitors of anandamide inactivation with cannabimimetic activity in vitro and in vivo. The Biochemical Journal. 2000 Nov 1;351 Pt 3:817-24. PMID 11042139 ^ Bisogno T, Ligresti A, Di Marzo V. The endocannabinoid signalling system: biochemical aspects. Pharmacology, Biochemistry, and Behavior. 2005 Jun;812:224-38. PMID 15935454 ^ Ralevic V. July 2003. Cannabinoid modulation of peripheral autonomic and sensory neurotransmission.. European journal of pharmacology 472 1-2: 1-21. doi:10.1016/S0014-29990301813-2. PMID 12860468. ^ Porter AC, Sauer JM, Knierman MD, Becker GW, Berna MJ, Bao J, Nomikos GG, Carter P, Bymaster FP, Leese AB, Felder CC. June 2002. Characterization of a Novel Endocannabinoid, Virodhamine, with Antagonist Activity at the CB1 Receptor. The Journal of pharmacology and experimental therapeutics 301 3: 1020-1024. doi:10.1124/jpet.301.3.1020. PMID 12023533. ^ Fride E, Bregman T, Kirkham TC. April 2005. Endocannabinoids and food intake: newborn suckling and appetite regulation in adulthood.. Experimental Biology and Medicine 230 4: 225-234. doi:10.1371/journal.pbio.0020286. PMID 15792943. ^ Nicoll RA, Alger BE 2004. The brain's own marijuana. Sci. Am. 291 6: 68-75. PMID 15597982. ^ http://www.marijuana.org/mydna10-12-05.htm Notes Elsohly MA, Slade D 2005. Chemical constituents of marijuana: the complex mixture of natural cannabinoids. Life Sci. 78 5: 539-48. doi:10.1016/j.lfs.2005.09.011. PMID 16199061. Hanus L 1987. Biogenesis of cannabinoid substances in the plant. Acta Universitatis Palackianae Olomucensis Facultatis Medicae 116: 47-53. PMID 2962461. HanuÅ¡ L., KrejÄ?à Z. Isolation of two new cannabinoid acids from Cannabis sativa L. of Czechoslovak origin. Acta Univ. Olomuc., Fac. Med. 74, 161-166 1975 HanuÅ¡ L., KrejÄ?à Z., Hruban L. Isolation of cannabidiolic acid from Turkish variety of cannabis cultivated for fibre. Acta Univ. Olomuc., Fac. Med. 74, 167-172 1975 Turner C. E., Mole M. L., HanuÅ¡ L., ElSohly H. N. Constituents of Cannabis sativa L. XIX. Isolation and structure elucidation of cannabiglendol. A novel cannabinoid from an Indian variant. J. Nat. Prod. - Lloydia 44 1, 27-33 1981 Devane WA, Hanus L, Breuer A, et al 1992. Isolation and structure of a brain constituent that binds to the cannabinoid receptor. Science 258 5090: 1946-9. doi:10.1126/science.1470919. PMID 1470919. Hanus L, Gopher A, Almog S, Mechoulam R 1993. Two new unsaturated fatty acid ethanolamides in brain that bind to the cannabinoid receptor. J. Med. Chem. 36 20: 3032-4. doi:10.1021/jm00072a026. PMID 8411021. Mechoulam R, Ben-Shabat S, Hanus L, et al 1995. Identification of an endogenous 2-monoglyceride, present in canine gut, that binds to cannabinoid receptors. Biochem. Pharmacol. 50 1: 83-90. doi:10.1016/0006-29529500109-D. PMID 7605349. External links The external links in this article may not follow 's content policies or guidelines. Please improve this article by removing excessive or inappropriate external links. Bela Szabo: Pharmacology of Cannabinoid Receptors, BIOTREND Reviews No. 02, February 2008 The International Cannabinoid Research Society Cannabinoids: A Secret History by Tom Geller, Chemical Heritage Newsmagazine, 25 2, Summer 2007 Pharmacokinetics and Disposition of Cannabinoids Stereochemical Requirements for Cannabimimetic Activity The Endocannabinoid System Network ECSN Cannabis Report 2002 Ministry of Public Health of Belgium Senate Report on Cannabis Canada - 2002 at the Parliament of Canada The Health and Psychological Effects of Cannabis Use Australia - Monograph 44 - 2001 at Department of Health and Ageing Australia Marijuana and Medicine - Assessing the Science Base Institute of Medicine - 1999 at National Academies Press House of Lords Report - Cannabis United Kingdom - 1998 at Parliament of the United Kingdom Cannabis: A Health Perspective and Research Agenda - 1997 at World Health Organization Overview of the Endocannabinoid Signalling System Chemical Ecology of Cannabis J. Intl. Hemp Assn. - 1994 What Every Doctor Should Know About Cannabinoids at California Cannabis Research Medical Group Therapeutic Potential in Spotlight at Cannabinoid Researchers' Meeting at California Cannabis Research Medical Group THC tetrahydrocannabinol accumulation in glands of Cannabis Cannabaceae Inheritance of Chemical Phenotype in Cannabis Sativa Genetics at Genetics Society of America Medicinal marijuana laws, policies and news Compounds found in Cannabis sativa Cannabinoids and the Brain - The most recent biomedical book on the endocannabinoid system v d e Cannabinoids Plant cannabinoids CBD CBDV CBN CBG CBV CBL THC THC-C4 THCV Cannabinoid metabolites 11-Hydroxy-THC 11-nor-9-Carboxy-THC Endogenous cannabinoids Arachidonoyl ethanolamide Anandamide or AEA 2-Arachidonoylglycerol 2-AG 2-Arachidonyl glyceryl ether noladin ether Virodhamine N-arachidonoyl-dopamine NADA; Oleamide Synthetic cannabinoid agonists Classical cannabinoids Dibenzopyrans A-41988 Ajulemic acid AM-087 AM-411 AM-855 AM-905 AM-906 AM-919 AM-938 AM-4030 AMG-1 AMG-3 AMG-36 AMG-41 Dexanabinol HU-211 DMHP Dronabinol HU-210 JWH-051 JWH-133 JWH-139 L-759,633 L-759,656 Levonantradol Nabilone Nabitan O-806 O-823 O-1057 O-1125 O-1238 O-2545 O-2694 Parahexyl THC-O-acetate THC-O-phosphate Nonclassical cannabinoids CP 47,497 CP 55,244 CP 55,940 HU-308 2-Isopropyl-5-methyl-1-2,6-dihydroxy-4-nonylphenylcyclohex-1-ene Aminoalkylindoles AM-630 AM-1241 JWH-015 JWH-018 JWH-073 JWH-081 JWH-200 L-768,242 Pravadoline WIN 55,212-2 Aminoalkylpyrroles JWH-030 JWH-147 JWH-307 Eicosanoids AM-883 Arachidonyl-2'-chloroethylamide Arachidonylcyclopropylamide Methanandamide O-585 O-689 O-1812 O-1860 O-1861 Others BAY 38-7271 BAY 59-3074 GW 842,166X JWH-171 O-2220 Endocannabinoid activity enhancers AM-404 CAY-10401 CAY-10402 N-arachidonoyl-serotonin O-1624 PF-622 PF-750 URB-597 URB-602 URB-754 Cannabinoid antagonists and inverse agonists AM-251 AM-281 AM-630 AVE-1625 BML-190 CAY-10508 CB-25 CB-52 JTE-907 LY-320,135 MK-9470 NESS-0327 O-1184 O-2050 O-2654 Rimonabant SLV-319 SR-144,528 Surinabant Taranabant VCHSR Retrieved from http://en..org/wiki/Cannabinoids#Endocannabinoids Categories: Analgesics | Cannabinoids | Cannabis | NeurochemistryHidden categories: All articles with statements | Articles with statements since October 2007 | Articles with statements since May 2008 | Articles with statements since September 2007 | external links cleanup Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages ÄŒesky Deutsch Español Français Italiano Nederlands 日本語 Polski РуÑ?Ñ?кий Suomi Svenska This page was last modified on 2 August 2008, at 21:50
39 Reasons to Drink Acai Juice Every Day
What is MonaVie - Watch the 8-minute video
Discovering MonaVie Video
The Power of You Video
Effects of MonaVie Active on Antioxidant Capacity in Humans
Log into your Wholesale MonaVie Account
So many of us do not eat a balanced diet, get enough sleep, have too much stress, or are impacted with toxins and pollutants. Drinking 2 ounces of MonaVie twice a day will help your body detoxify as well as build your immune system. Its the smartest thing you can do for yourself, so start today. Buying MonaVie through our company guarantees you support 7 days a week and, if you would like to share MonaVie with your family and friends we will guide you from start to finish.
1. Click on Enroll Now (30 - 55% off retail price)
2. Pay $39 for your Wholesale ID number.
3. NO minimum order required.
4. MonaVie is delivered to your door in 3 to 5 days.