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Cannabinoids 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.[1] 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.

Cannabinoid receptors Edit

Main article: cannabinoid receptor

Before the 1980's, 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. CB2 receptors appear to be responsible for the anti-inflammatory and possibly other therapeutic effects of cannabis.

Phytocannabinoids Edit

Type Skeleton Cyclization
Cannabigerol-type
CBG
CBG-type cannabinoid CBG-type cyclization of cannabinoids
Cannabichromene-type
CBC
CBC-type cannabinoid CBC-type cyclization of cannabinoids
Cannabidiol-type
CBD
CBD-type cannabinoid CBD-type cyclization of cannabinoids
Tetrahydrocannabinol-
and
Cannabinol-type
THC, CBN
CBN-type cannabinoid CBN-type cyclization of cannabinoids
Cannabielsoin-type
CBE
CBE-type cannabinoid CBE-type cyclization of cannabinoids
iso-
Tetrahydrocannabinol-
type
iso-THC
Iso-CBN-type cannabinoid Iso-CBN-type cyclization of cannabinoids
Cannabicyclol-type
CBL
CBL-type cannabinoid CBL-type cyclization of cannabinoids
Cannabicitran-type
CBT
CBT-type cannabinoid 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 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).

TypesEdit

At least 66 cannabinoids have been isolated from the cannabis plant[2] 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 ones are listed below:

TetrahydrocannabinolEdit

Main article: 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.[3] Its effects are perceived to be more cerebral.[How to reference and link to summary or text]

delta-9-Tetrahydrocannabinol9-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.

CannabidiolEdit

Main article: cannabidiol

CBD is not psychoactive, and neither does it affect the psychoactivity of THC[4].

Medically, it appears to relieve convulsion, inflammation, anxiety, and nausea.[How to reference and link to summary or text] CBD has a greater affinity for the CB2 receptor than for the CB1 receptor. It is perceived to have more effect on the body.[How to reference and link to summary or text]

CBD shares a precursor with THC and is the main cannabinoid in low-THC Cannabis strains.

CannabinolEdit

Main article: 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, and is perceived to be sedative or stupefying.[How to reference and link to summary or text]

TetrahydrocannabivarinEdit

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.[5]

CannabichromeneEdit

Main article: Cannabichromene

Cannabichromene (CBC) is non-psychoactive and does not affect the psychoactivity of THC,[4] a precursor of CBD and THC.

Double bond positionEdit

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.

LengthEdit

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 profileEdit

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 have been created. [How to reference and link to summary or text]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.

PharmacologyEdit

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.

ProductionEdit

Production of cannabinoids include both the synthesis in the plant, and separation of certain types from this material.

Plant synthesisEdit

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.

SeparationEdit

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.

HistoryEdit

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 Edit

For more details on this topic, see Endocannabinoid system.
File:Rnt Anandamide.jpg

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 ligandsEdit

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.[6] It is found in nearly all tissues in a wide range of animals.[How to reference and link to summary or text]

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 seeds[7] and in molluscs.[8]

Another endocannabinoid, 2-arachidonoyl glycerol, binds to both the CB1 and CB2 receptors with similar affinity, acting as a full agonist at both.[6] 2-AG is present at significantly higher concentrations in the brain than anandamide[9], and there is some controversy over whether 2-AG rather than anandamide is chiefly responsible for endocannabinoid signalling in vivo[10]. 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.[11]

In 2001 a third, ether-type endocannabinoid, 2-arachidonyl glyceryl ether (noladin ether), was isolated from porcine brain. [12] 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.[13] 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.[6]

Discovered in 2000, NADA preferentially binds to the CB1 receptor.[14] Like anandamide, NADA is also an agonist for the vanilloid receptor subtype 1 (TRPV1), a member of the vanilloid receptor family.[15][16]

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.[17]

FunctionEdit

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.[18]

Retrograde signalEdit

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.

RangeEdit

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 thoughtsEdit

Endocannabinoids constitute a versatile system for affecting neuronal network properties in the nervous system.

Scientific American published an article in December of 2004, entitled "The Brain's Own Marijuana" discussing the endogenous cannabinoid system. [19]

The current understanding recognizes the role that endocannabinoids play in almost every major life function in the human body.[How to reference and link to summary or text] 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.

Synthetic & Patented Cannabinoids Edit

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:


Other notable synthetic cannabinoids include:

Table of natural cannabinoids Edit

Cannabigerol-type (CBG)
Cannabigerol

Cannabigerol
(E)-CBG-C5

Cannabigerol monomethyl ether

Cannabigerol
monomethyl ether
(E)-CBGM-C5 A

Cannabinerolic acid A

Cannabinerolic acid A
(Z)-CBGA-C5 A

Cannabigerovarin

Cannabigerovarin
(E)-CBGV-C3

Cannabigerolic acid A

Cannabigerolic acid A
(E)-CBGA-C5 A

Cannabigerolic acid A monomethyl ether

Cannabigerolic acid A
monomethyl ether
(E)-CBGAM-C5 A

Cannabigerovarinic acid A

Cannabigerovarinic acid A
(E)-CBGVA-C3 A

Cannabichromene-type (CBC)
Cannabichromene

(±)-Cannabichromene
CBC-C5

Cannabichromenic acid A

(±)-Cannabichromenic acid A
CBCA-C5 A

Cannabichromevarine

(±)-Cannabivarichromene, (±)-Cannabichromevarin
CBCV-C3

Cannabichromevarinic acid A

(±)-Cannabichromevarinic
acid A
CBCVA-C3 A

Cannabidiol-type (CBD)
Cannabidiol

(−)-Cannabidiol
CBD-C5

Cannabidiol momomethyl ether

Cannabidiol
momomethyl ether
CBDM-C5

Cannabidiol-C4

Cannabidiol-C4
CBD-C4

Cannabidivarin

(−)-Cannabidivarin
CBDV-C3

Cannabidiorcol

Cannabidiorcol
CBD-C1

Cannabidiolic acid

Cannabidiolic acid
CBDA-C5

Cannabidivarinic acid

Cannabidivarinic acid
CBDVA-C3

Cannabinodiol-type (CBND)
Cannabinodiol

Cannabinodiol
CBND-C5

Cannabinodivarin

Cannabinodivarin
CBND-C3

Tetrahydrocannabinol-type (THC)
Delta-9-tetrahydrocannabinol

Δ9-Tetrahydrocannabinol
Δ9-THC-C5

Delta-9-tetrahydrocannabinol-C4

Δ9-Tetrahydrocannabinol-C4
Δ9-THC-C4

Delta-9-tetrahydrocannabivarin

Δ9-Tetrahydrocannabivarin
Δ9-THCV-C3

Tetrahydrocannabiorcol

Δ9-Tetrahydrocannabiorcol
Δ9-THCO-C1

Delta-9-tetrahydrocannabinolic acid A

Δ9-Tetrahydro-
cannabinolic acid A
Δ9-THCA-C5 A

Delta-9-tetrahydrocannabinolic acid B

Δ9-Tetrahydro-
cannabinolic acid B
Δ9-THCA-C5 B

Delta-9-tetrahydrocannabinolic acid-C4

Δ9-Tetrahydro-
cannabinolic acid-C4
A and/or B
Δ9-THCA-C4 A and/or B

Delta-9-tetrahydrocannabivarinic acid A

Δ9-Tetrahydro-
cannabivarinic acid A
Δ9-THCVA-C3 A

Delta-9-tetrahydrocannabiorcolic acid

Δ9-Tetrahydro-
cannabiorcolic acid
A and/or B
Δ9-THCOA-C1 An and/or B

Delta-8-tetrahydrocannabinol

(−)-Δ8-trans-(6aR,10aR)-
Δ8-Tetrahydrocannabinol
Δ8-THC-C5

Delta-8-tetrahydrocannabinolic acid A

(−)-Δ8-trans-(6aR,10aR)-
Tetrahydrocannabinolic
acid A
Δ8-THCA-C5 A

Cis-delta-9-tetrahydrocannabinol

(−)-(6aS,10aR)-Δ9-
Tetrahydrocannabinol
(−)-cis9-THC-C5

Cannabinol-type (CBN)
Cannabinol

Cannabinol
CBN-C5

Cannabinol-C4

Cannabinol-C4
CBN-C4

Cannabivarin

Cannabivarin
CBN-C3

Cannabinol-C2

Cannabinol-C2
CBN-C2

Cannabiorcol

Cannabiorcol
CBN-C1

Cannabinolic acid A

Cannabinolic acid A
CBNA-C5 A

Cannabinol methyl ether

Cannabinol methyl ether
CBNM-C5

Cannabitriol-type (CBT)
(-)-trans-cannabitriol

(−)-(9R,10R)-trans-
Cannabitriol
(−)-trans-CBT-C5

(+)-trans-cannabitriol

(+)-(9S,10S)-Cannabitriol
(+)-trans-CBT-C5

Cis-cannabitriol

(±)-(9R,10S/9S,10R)-
Cannabitriol
(±)-cis-CBT-C5

Trans-cannabitriol ethyl ether

(−)-(9R,10R)-trans-
10-O-Ethyl-cannabitriol
(−)-trans-CBT-OEt-C5

Trans-cannabitriol-C3

(±)-(9R,10R/9S,10S)-
Cannabitriol-C3
(±)-trans-CBT-C3

8,9-dihydroxy-delta-6a(10a)-tetrahydrocannabinol

8,9-Dihydroxy-Δ6a(10a)-
tetrahydrocannabinol
8,9-Di-OH-CBT-C5

Cannabidiolic acid A cannabitriol ester

Cannabidiolic acid A
cannabitriol ester
CBDA-C5 9-OH-CBT-C5 ester

Cannabiripsol

(−)-(6aR,9S,10S,10aR)-
9,10-Dihydroxy-
hexahydrocannabinol,
Cannabiripsol
Cannabiripsol-C5

Cannabitetrol

(−)-6a,7,10a-Trihydroxy-
Δ9-tetrahydrocannabinol
(−)-Cannabitetrol

10-oxo-delta-6a(10a)-tetrahydrocannabinol

10-Oxo-Δ6a(10a)-
tetrahydrocannabinol
OTHC

Cannabielsoin-type (CBE)
Cannabielsoin

(5aS,6S,9R,9aR)-
Cannabielsoin
CBE-C5

C3-cannabielsoin

(5aS,6S,9R,9aR)-
C3-Cannabielsoin
CBE-C3

Cannabielsoic acid A

(5aS,6S,9R,9aR)-
Cannabielsoic acid A
CBEA-C5 A

Cannabielsoic acid B

(5aS,6S,9R,9aR)-
Cannabielsoic acid B
CBEA-C5 B

C3-cannabielsoic acid B

(5aS,6S,9R,9aR)-
C3-Cannabielsoic acid B
CBEA-C3 B

Cannabiglendol-C3

Cannabiglendol-C3
OH-iso-HHCV-C3

Dehydrocannabifuran

Dehydrocannabifuran
DCBF-C5

Cannabifuran

Cannabifuran
CBF-C5

Isocannabinoids
Delta-7-trans-isotetrahydrocannabinol

(−)-Δ7-trans-(1R,3R,6R)-
Isotetrahydrocannabinol

Delta-7-cis-isotetrahydrocannabivarin

(±)-Δ7-1,2-cis-
(1R,3R,6S/1S,3S,6R)-
Isotetrahydro-
cannabivarin

Delta-7-trans-isotetrahydrocannabivarin

(−)-Δ7-trans-(1R,3R,6R)-
Isotetrahydrocannabivarin

Cannabicyclol-type (CBL)
Cannabicyclol

(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclol
CBL-C5

Cannabicyclolic acid A

(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclolic acid A
CBLA-C5 A

Cannabicyclovarin

(±)-(1aS,3aR,8bR,8cR)-
Cannabicyclovarin
CBLV-C3

Cannabicitran-type (CBT)
Cannabicitran

Cannabicitran
CBT-C5

Cannabichromanone-type (CBCN)
Cannabichromanone

Cannabichromanone
CBCN-C5

Cannabichromanone-C3

Cannabichromanone-C3
CBCN-C3

Cannabicoumaronone

Cannabicoumaronone
CBCON-C5

See alsoEdit

Cited SourcesEdit

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References Edit

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