Size | Seeds | Peers | Completed |
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Cannabinoid Profiles - THC, THCA, THCV, CBD, CBG, CBN, CBC & Terpenes.
Video Description:
Brought to you by SC Laboratories and WeedMaps.tv in California. Health Professionals are from CannaCenters Research California. Profiles include: THC – Delta-9 Tetrahydrocannabinol, THCA – Tetrahydrocannabinolic Acid, THCV – Tetrahydrocannabivarin, CBD – Cannabidiol, CBN – Cannabinol, CBG – Cannabigerol, CBC – Cannabichromene, Terpenes – diverse group of organic HydroCarbons (C5H8).
Watch online:
http://www.youtube.com/watch?v=eeHmmlm_2Po
Other information:
Cannabinoids - What are Cannabinoids?
Cannabinoids are a group of terpenophenolic compounds present in Cannabis (''Cannabis sativa'') and occur naturally in the nervous and immune systems of animals.
The broader definition of cannabinoids refers 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, quinolines and arylsulphonamides, and additional compounds that do not fall into these standard classes but bind to cannabinoid receptors.
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.
At the present time, 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.
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.
At present, there are two known types of cannabinoid receptors, termed CB1 and CB2, with mounting evidence of more.
Cannabinoid receptor type 1
CB1 receptors are found primarily in the brain, to be specific 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 absent in the medulla oblongata, the part of the brain stem 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.
Cannabinoid receptor type 2
CB2 receptors are almost exclusively found in the immune system, with the greatest density in the spleen.
While found only in the peripheral nervous system, a report does indicate that CB2 is expressed by a subpopulation of microglia in the human cerebellum.
CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.
Phytocannabinoids
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 plant 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
Tetrahydrocannabinol (THC) is the primary psychoactive component of the plant. It appears to ease moderate pain (analgetic) and to be neuroprotective. THC has approximately equal affinity for the CB1 and CB2 receptors. Its effects are perceived to be more cerebral.
''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
Cannabidiol (CBD) is not psychoactive, and was thought not to affect the psychoactivity of THC. However, recent evidence shows that smokers of cannabis with a higher CBD/THC ratio were less likely to experience schizophrenia-like symptoms.
This is supported by psychological tests, in which participants experience less intense psychotic effects when intravenous THC was co-administered with CBD (as measured with a PANSS test).
It has been hypothesized that CBD acts as an allosteric antagonist at the CB1 receptor and thus alters the psychoactive effects of THC.
It appears to relieve convulsion, inflammation, anxiety, and nausea. CBD has a greater affinity for the CB2 receptor than for the CB1 receptor.
Cannabigerol
Cannabigerol (CBG) is non-psychotomimetic but still affects the overall effects of Cannabis. It acts as an α2-adrenergic receptor agonist, 5-HT1A receptor antagonist, and CB1 receptor antagonist. It also binds to the CB2 receptor.
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.
Cannabichromene
Cannabichromene (CBC) is non-psychoactive and does not affect the psychoactivity of THC It is found in nearly all tissues in a wide range of animals.
Two analogs of anandamide, 7,10,13,16-docosatetraenoylethanolamide and ''homo''-γ-linolenoylethanolamine, have similar pharmacology.
All of these are members of a family of signalling lipids called ''N''-acylethanolamides, which also includes the noncannabimimetic palmitoylethanolamide and oleoylethanolamine, which possess anti-inflammatory and orexigenic effects, respectively. Many ''N''-acylethanolamines have also been identified in plant seeds and in molluscs.
•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, and there is some controversy over whether 2-AG rather than anandamide is chiefly responsible for endocannabinoid signalling ''in vivo''.
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.
•2-arachidonyl glyceryl ether (noladin ether)
In 2001, a third, ether-type endocannabinoid, 2-arachidonyl glyceryl ether (noladin ether), was isolated from porcine brain.
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.
It binds to the CB1 cannabinoid receptor (''K''i = 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.
Like anandamide, NADA is also an agonist for the vanilloid receptor subtype 1 (TRPV1), a member of the vanilloid receptor family.
•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.
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 and 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.
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 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.
On the converse, 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.
The current understanding recognizes the role that endocannabinoids play in almost every major life function in the human body.
U.S. Patent # 6630507
In 2003 The U.S.A.'s Government as represented by the Department of Health and Human Services 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 THC
•HU-331 a potential anti-cancer drug derived from cannabidiol that specifically inhibits topoisomerase II.
•SR144528, a CB2 receptor antagonists
•WIN 55, 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