Cannabis Chemistry

This thread is dedicated to understanding the bio-chemical processes of cannabis plants and their interactions with the human body. Most, if not all the information i'll be pasting is research/articles from public domain sources (thats code for ive copied a whole bunch of info from wikipedia lol), which hopefully means im not breaking any copyright laws, if i come across the same with an author ill be sure to reference it.  Iv'e included a link to the original webpage so reference to the original authors can be made if anyone using this info for essays, webpages with their own work ect. 
Feel free to contribute to this thread!  
I love chemistry and the bio-chemical processes of the world and cannabis. So if you wish to learn more about the biochemistry of cannabis like me start reading.   
\n\nhttp://en.wikipedia.org/wiki/Tetrahydrocannabinolic_acid
\tTetrahydrocannabinolic acid 
(THCA, 2-COOH-THC), is a biosynthetic precursor of tetrahydrocannabinol (THC), the active component of Cannabis.^[1]^[2]^[3]^[4] THCA is found in variable quantities in fresh, undried cannabis, but is progressively decarboxylated to THC with drying, and especially under intense heating such as when cannabis is smoked.^[5] While THCA does not have psychoactive effects in its own right, it does have antiinflammatory and neuroprotective effects.^[6]^[7] Despite the ready decarboxylation by drying or heating ex vivo, conversion of THCA to THC in vivo appears to be very limited, giving it only very slight efficacy as a prodrug for THC.^[8] Consequently it is believed to be important in less-psychoactive preparations of cannabis used for medical use, such as cannabis tea.^[9] It is also commonly used as a biomarker in drug testing along with THCV, to distinguish between prescribed processed forms of medicinal cannabis such as Marinol, and cannabis plant material which may also be used by patients.^[10]
\n\n\n\t \thttp://en.wikipedia.org/wiki/CannabinoidsPhytocannabinoids
Phytocannabinoids (also called natural cannabinoids, herbal cannabinoids, and classical cannabinoids) are known to occur in several different plant species. These include Cannabis sativa, Cannabis indica, Cannabis ruderalis, Echinacea purpurea, Echinacea angustifolia, Echinacea pallida, Acmella oleracea, Helichrysum umbraculigerum, and Radula marginata.^[10] The best known herbal cannabinoids are Δ9-tetrahydrocannabinol (THC) from Cannabis and the lipophilic alkamides (alkylamides) from Echinacea species.^[10]
At least 85 different cannabinoids have been isolated from the Cannabis plant^[11] and 25 different cannabinoids from Echinacea species.^[12] In Cannabis, these cannabinoids are concentrated in a viscous resin produced in structures known as glandular trichomes. In Echinacea species, cannabinoids are found throughout the plant structure, but are most concentrated in the roots and stems.^[13] Tea (Camellia sinensis) catechins have an affinity for human cannabinoid receptors.^[14]
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).
\n\n 
http://en.wikipedia.org/wiki/Cannabinoids  <(Refer to this webpage for the structure of the following molecules.)
\tCannabis-derived cannabinoids[SIZE=small][edit][/SIZE]\tTypes[SIZE=small][edit][/SIZE]To the right, the main classes of cannabinoids from Cannabis are shown. All classes derive from cannabigerol-type compounds and differ mainly in the way this precursor is cyclized.
Tetrahydrocannabinol (THC), cannabidiol (CBD), cannabinol (CBN) (derived from Cannabis); and dodeca-2E,4E,8Z,10E/Z-tetraenoic-acid-isobutylamides (the main bioactive constituents from Echinacea species) are the most prevalent natural cannabinoids and have received the most study.

• CBG (Cannabigerol)
• CBC (Cannabichromene)
• CBL (Cannabicyclol)
• CBV (Cannabivarin)
• THCV (Tetrahydrocannabivarin)
• CBDV (Cannabidivarin)
• CBCV (Cannabichromevarin)
• CBGV (Cannabigerovarin)
• CBGM (Cannabigerol Monomethyl Ether)

 
 
\tTetrahydrocannabinol[SIZE=small][edit][/SIZE]Main article: Tetrahydrocannabinol
Tetrahydrocannabinol (THC) is the primary psychoactive component of the Cannabis plant. Delta-9-tetrahydrocannabinol (Δ⁹-THC, THC) and delta-8-tetrahydrocannabinol (Δ⁸-THC), mimic the action of anandamide, a neurotransmitter produced naturally in the body. These two THC's produce the effects associated with cannabis by binding to the CB[SUB]1[/SUB] cannabinoid receptors in the brain. THC appears to ease moderate pain (analgesic) and to be neuroprotective. Studies show THC reduces neuroinflammation and stimulates neurogenesis.^[15]^[16]^[17] THC has approximately equal affinity for the CB[SUB]1[/SUB] and CB[SUB]2[/SUB] receptors.^[18]
\n\n\tCannabidiol[SIZE=small][edit][/SIZE]Main article: Cannabidiol
Cannabidiol (CBD) is not psychoactive, and was thought not to affect the psychoactivity of THC.^[19] However, recent evidence shows that smokers of cannabis with a higher CBD/THC ratio were less likely to experience schizophrenia-like symptoms.^[20] This is supported by psychological tests, in which participants experience less intense psychotic-like effects when intravenous THC was co-administered with CBD (as measured with a PANSS test).^[21] Cannabidiol has little affinity for CB[SUB]1[/SUB] and CB[SUB]2[/SUB]receptors but acts as an indirect antagonist of cannabinoid agonists.^[22] Recently it was found to be an antagonist at the putative new cannabinoid receptor, GPR55, aGPCR expressed in the caudate nucleus and putamen.^[23] Cannabidiol has also been shown to act as a 5-HT[SUB]1A[/SUB] receptor agonist,^[24] an action that is involved in itsantidepressant,^[25]^[26] anxiolytic,^[26]^[27] and neuroprotective^[28]^[29] effects.
It appears to relieve convulsion, inflammation, anxiety, and nausea.^[30] CBD has a greater affinity for the CB[SUB]2[/SUB] receptor than for the CB[SUB]1[/SUB] receptor.^[30]
CBD shares a precursor with THC and is the main cannabinoid in low-THC Cannabis strains. CBD apparently plays a role in preventing the short-term memory loss associated with THC in mammals.
Some research suggests that the antipsychotic effects of cannabidiol potentially represent a novel mechanism in the treatment of schizophrenia.^[31]
Researchers at California Pacific Medical Center discovered CBD's ability to "turn off" the activity of ID1, the gene responsible for metastasis in breast and other types of cancers, including the particularly aggressive triple negative breast cancer.^[32]^[33]^[34] The researchers hope to start human trials soon.^[35]
\n\n\tCannabinol[SIZE=small][edit][/SIZE]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. Its affinity to the CB[SUB]2[/SUB] receptor is higher than for the CB[SUB]1[/SUB] receptor.^[36]
\n\n\tCannabigerol[SIZE=small][edit][/SIZE]Main article: Cannabigerol
Cannabigerol (CBG) is non-psychotomimetic but still affects the overall effects of Cannabis. It acts as an Î±[SUB]2[/SUB]-adrenergic receptor agonist, 5-HT[SUB]1A[/SUB] receptor antagonist, and CB[SUB]1[/SUB] receptor antagonist.^[37] It also binds to the CB[SUB]2[/SUB] receptor.^[37]
\n\tTetrahydrocannabivarin[SIZE=small][edit][/SIZE]Main article: Tetrahydrocannabivarin
Tetrahydrocannabivarin (THCV) is prevalent in certain central Asian and southern African strains of Cannabis.^[38]^[39] It is an antagonist of THC at CB[SUB]1[/SUB] receptors and attenuates the psychoactive effects of THC.^[40]
\n\tCannabidivarin[SIZE=small][edit][/SIZE]Main article: Cannabidivarin
Although cannabidivarin (CBDV) is usually a minor constituent of the cannabinoid profile, enhanced levels of CBDV have been reported in feral cannabis plants from the northwest Himalayas, and in hashish from
Nepal.^[41]^[39]
\n\n\tCannabichromene[SIZE=small][edit][/SIZE]Main article: Cannabichromene
Cannabichromene (CBC) is non-psychoactive and does not affect the psychoactivity of THC .^[19]
\n\n\tDouble bond position[SIZE=small][edit][/SIZE]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 Δ⁹-THC, while the minor form is called Δ⁸-THC. Under the alternate terpene numbering system, these same compounds are called Δ¹-THC and Δ⁶-THC, respectively.
\n\n\tLength[SIZE=small][edit][/SIZE]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.
\n\n\tCannabis plant profile[SIZE=small][edit][/SIZE]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 that 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.
Quantitative analysis of a plant's cannabinoid profile is often determined by gas chromatography (GC), or more reliably by gas chromatography combined with mass spectrometry (GC/MS). Liquid chromatography (LC) techniques are also possible, and, unlike GC methods, can differentiate between the acid and neutral forms of the cannabinoids. 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.
\n\n\tPharmacology[SIZE=small][edit][/SIZE]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. Δ⁹-THC is metabolized to 11-hydroxy-Δ⁹-THC, which is then metabolized to 9-carboxy-THC. Some cannabis metabolites can be detected in the body several weeks after administration. These metabolites are the chemicals recognized by common antibody-based "drug tests"; in the case of THC et al., these loads do not represent intoxication (compare to ethanol breath tests that measure instantaneous blood alcohol levels) but an integration of past consumption over an approximately month-long window.
\n\n\tPlant synthesis[SIZE=small][edit][/SIZE]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. CBD is then enzymatically cyclized to THC. For the propyl homologues (THCV, CBDV and CBNV), there is a similar pathway that is based on CBGV. Recent studies^[which?] show that THC is not cyclized from CBD but rather directly from CBG. No experiment thus far has turned up an enzyme that converts CBD into THC, although it is still hypothesized^{[by whom?]}.
\n\n\tSeparation[SIZE=small][edit][/SIZE]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. Butane may be used, which evaporates extremely quickly. Supercritical solvent extraction with carbon dioxide is an alternative technique. Although this process requires high pressures (73 atmospheres or more), 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.
\n\n\n\tNatural occurrence[SIZE=small][edit][/SIZE]Main article: Medical_cannabis#Difference between C. indica and C. sativa
Cannabis indica may have a CBD:THC ratio 4–5 times that of Cannabis sativa.
\n\n\tHistory[SIZE=small][edit][/SIZE]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, CBD was originally believed to be a natural precursor to THC. However, it is now known that CBD and THC are produced independently in the cannabis plant from the precursor CBG.
 
 
 
 
http://en.wikipedia.org/wiki/Cannabinoids\tSynthetic cannabinoids[SIZE=small][edit][/SIZE]
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 22 countries including England, Canada and Spain. Sativex develops whole-plant cannabinoid medicines
• Rimonabant (SR141716), a selective cannabinoid (CB[SUB]1[/SUB]) receptor inverse agonist once used as an anti-obesity drug under the proprietary name Acomplia. It was also used for smoking cessation

Other notable^[why?] synthetic cannabinoids include:

• JWH-018, a potent synthetic cannabinoid agonist discovered by Dr. John W. Huffman at Clemson University. It is being increasingly sold in legal smoke blends collectively known as "spice". Several countries and states have moved to ban it legally.
• JWH-073
• 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^[58]
• HU-331 a potential anti-cancer drug derived from cannabidiol that specifically inhibits topoisomerase II.
• SR144528, a CB[SUB]2[/SUB] receptor antagonist
• WIN 55,212-2, a potent cannabinoid receptor agonist
• JWH-133, a potent selective CB[SUB]2[/SUB] receptor agonist
• Levonantradol (Nantrodolum), an anti-emetic and analgesic but not currently in use in medicine
• AM-2201, a potent cannabinoid receptor agonist.

 
 
 
 
 
 
 
The following is information relating to cannabinoid recoptors and their role in every potheads body
 
 
http://en.wikipedia.org/wiki/Cannabinoid_receptor and http://en.wikipedia.org/wiki/Cannabinoids
 
\t The cannabinoid receptors are a class of cell membrane receptors under the G protein-coupled receptor superfamily.^[1]^[2]^[3] As is typical of G protein-coupled receptors, the cannabinoid receptors contain seven transmembrane spanning domains.^[4] Cannabinoid receptors are activated by three major groups of ligands, endocannabinoids (produced by the mammalian body), plant cannabinoids (such as THC, produced by the cannabis plant) and synthetic cannabinoids (such as HU-210). All of the endocannabinoids and plant cannabinoids are lipophilic, i.e. fat soluble, compounds.
There are currently two known subtypes, termed CB[SUB]1[/SUB] and CB[SUB]2[/SUB].^[5]^[6] The CB[SUB]1[/SUB] receptor is expressed mainly in the brain (central nervous system or "CNS"), but also in the lungs, liver and kidneys. The CB[SUB]2[/SUB]receptor is expressed mainly in the immune system and in hematopoietic cells.^[7] Mounting evidence suggests that there are novel cannabinoid receptors^[8] that is, non-CB[SUB]1[/SUB] and non-CB[SUB]2[/SUB], which are expressed in endothelial cells and in the CNS. In 2007, the binding of several cannabinoids to a G protein-coupled receptor (GPCR) in the brain was described.^[9]
The protein sequences of CB[SUB]1[/SUB] and CB[SUB]2[/SUB] receptors are about 44% similar.^[10] When only the transmembrane regions of the receptors are considered, amino acid similarity between the two receptor subtypes is approximately 68%.^[4] In addition, minor variations in each receptor have been identified. Cannabinoids bind reversibly and stereo-selectively to the cannabinoid receptors. The affinity of an individual cannabinoid to each receptor determines the effect of that cannabinoid. Cannabinoids that bind more selectively to certain receptors are more desirable for medical usage.
\n\n\n\t \tCB[SUB]1[/SUB]\tMain article: Cannabinoid receptor type 1Cannabinoid receptor type 1 (CB[SUB]1[/SUB]) receptors are thought to be one of the most widely expressed G protein-coupled receptors in the brain. This is due to endocannabinoid-mediated depolarization-induced suppression of inhibition, a very common form of short-term plasticity in which the depolarization of a single neuron induces a reduction in GABA-mediated neurotransmission. Endocannabinoids released from the depolarized post-synaptic neuron bind to CB[SUB]1[/SUB] receptors in the pre-synaptic neuron and cause a reduction in GABA release.
They are also found in other parts of the body. For instance, in the liver, activation of the CB[SUB]1[/SUB] receptor is known to increase de novo lipogenesis.^[11] Activation of presynaptic CB[SUB]1[/SUB] receptors is also known to inhibit sympathetic innervation of blood vessels and contributes to the suppression of the neurogenic vasopressor response in septic shock.^[12]
A 2004 study suggested that the endocannabinoids and their cannabinoid receptors play a major role during pre- and postnatal development. ^[13]
A study done on CB[SUB]1[/SUB] knockout mice (genetically altered mice that cannot produce CB[SUB]1[/SUB]) showed an increase in mortality rate. They also displayed suppressed locomotor activity as well as hypoalgesia (decreased pain sensitivity). The CB[SUB]1[/SUB] knockout mice did respond to Δ⁹-tetrahydrocannabinol, or THC. This shows that either CB[SUB]2[/SUB] or unknown cannabinoid receptors also have pharmacologic significance.^[14]
\n\n\n\tCB[SUB]2[/SUB][SIZE=small][edit][/SIZE]\t Main article: Cannabinoid receptor type 2
CB[SUB]2[/SUB] receptors are mainly expressed on T cells of the immune system, on macrophages and B cells, and in hematopoietic cells. They also have a function in keratinocytes, and are expressed on mousepre-implantation embryos. They are also expressed on peripheral nerve terminals. These receptors play a role in antinociception, or the relief of pain. In the brain, they are mainly expressed by microglial cells, where their role remains unclear. While the most likely cellular targets and executors of the CB[SUB]2[/SUB] receptor-mediated effects of endocannabinoids or synthetic agonists are the immune and immune-derived cells (e.g. leukocytes, various populations of T and B lymphocytes, monocytes/macrophages, dendritic cells, mast cells, microglia in the brain, Kupffer cells in the liver, etc.), the number of other potential cellular targets is expanding, now including endothelial and smooth muscle cells, fibroblasts of various origins, cardiomyocytes, and certain neuronal elements of the peripheral or central nervous systems.^[7]
\n\n\n\n\tOther cannabinoid receptors[SIZE=small][edit][/SIZE]\t The existence of additional cannabinoid receptors has long been suspected, due to the actions of compounds such as abnormal cannabidiol that produce cannabinoid-like effects on blood pressure and inflammation, yet do not activate either CB[SUB]1[/SUB] or CB[SUB]2[/SUB].^[15]^[16]^[17] Recent research strongly supports the hypothesis that the N-arachidonoyl glycine (NAGly) receptor GPR18 is the molecular identity of the abnormal cannabidiol receptor and additionally suggests that NAGly, the endogenous lipid metabolite of anandamide (also known as arachidonoylethanolamide or AEA), initiates directed microglial migration in the CNS through activation of GPR18.^[18] Other molecular biology studies have suggested that the orphan receptor GPR55 should in fact be characterised as a cannabinoid receptor, on the basis of sequence homology at the binding site. Subsequent studies showed that GPR55 does indeed respond to cannabinoid ligands.^[9]^[19] This profile as a distinct non-CB[SUB]1[/SUB]/CB[SUB]2[/SUB] receptor that responds to a variety of both endogenous and exogenous cannabinoid ligands, has led some groups to suggest GPR55 should be categorized as the CB[SUB]3[/SUB] receptor, and this re-classification may follow in time.^[20] However this is complicated by the fact that another possible cannabinoid receptor has been discovered in the hippocampus, although its gene has not yet been cloned,^[21] suggesting that there may be at least two more cannabinoid receptors to be discovered, in addition to the two that are already known. GPR119 has been suggested as a fifth possible cannabinoid receptor.^[22]
\n\n\n\tSignaling[SIZE=small][edit][/SIZE]\t Cannabinoid receptors are activated by cannabinoids, generated naturally inside the body (endocannabinoids) or introduced into the body as cannabis or a related synthetic compound.
After the receptor is engaged, multiple intracellular signal transduction pathways are activated. At first, it was thought that cannabinoid receptors mainly inhibited the enzyme adenylate cyclase (and thereby the production of the second messengermolecule cyclic AMP), and positively influenced inwardly rectifying potassium channels (=Kir or IRK).^[23] However, a much more complex picture has appeared in different cell types, implicating other potassium ion channels, calcium channels, protein kinase A and C, Raf-1, ERK, JNK, p38, c-fos, c-jun and many more.^[23]
Separation between the therapeutically undesirable psychotropic effects, and the clinically desirable ones, however, has not been reported with agonists that bind to cannabinoid receptors. THC, as well as the two major endogenous compounds identified so far that bind to the cannabinoid receptors -anandamide and 2-arachidonylglycerol (2-AG)- produce most of their effects by binding to both the CB[SUB]1[/SUB] and CB[SUB]2[/SUB] cannabinoid receptors. While the effects mediated by CB[SUB]1[/SUB], mostly in the central nervous system, have been thoroughly investigated, those mediated by CB[SUB]2[/SUB] are not equally well defined.
\n\n\n\n\tPhysiology[SIZE=small][edit][/SIZE]\tGastrointestinal activity[SIZE=small][edit][/SIZE]\t Inhibition of gastrointestinal activity has been observed after administration of Δ⁹-THC, or of anandamide. This effect has been assumed to be CB[SUB]1[/SUB]-mediated since the specific CB[SUB]1[/SUB] antagonist SR 141716A (Rimonabant) blocks the effect. Another report, however, suggests that inhibition of intestinal motility may also have a CB[SUB]2[/SUB]-mediated component.^[24]
\n\n\tCardiovascular activity[SIZE=small][edit][/SIZE]\t Cannabinoids are well known for their cardiovascular activity. Activation of peripheral CB[SUB]1[/SUB] receptors contributes to hemorrhagic and endotoxin-induced hypotension. Anandamide and 2-AG, produced by macrophages and platelets respectively, may mediate this effect.
The hypotension in hemorrhaged rats was prevented by the CB[SUB]1[/SUB] antagonist SR 141716A. Recently the same group found that anandamide-induced mesenteric vasodilation is mediated by an endothelially located SR 141716A-sensitive "anandamide receptor," distinct from the CB[SUB]1[/SUB] cannabinoid receptor, and that activation of such a receptor by an endocannabinoid, possibly anandamide, contributes to endotoxin-induced mesenteric vasodilation in vivo. The highly potent synthetic cannabinoid HU-210, as well as 2-AG, had no mesenteric vasodilator activity. Furthermore it was shown that mesenteric vasodilation by anandamide apparently has 2 components, one mediated by a SR 141716-sensitive non-CB[SUB]1[/SUB] receptor (located on the endothelium) and the other by an SR 141716A-resistant direct action on vascular smooth muscle.
The production of 2-AG is enhanced in normal, but not in endothelium-denuded rat aorta on stimulation with Carbachol, an acetylcholine receptor agonist. 2-AG potently reduces blood pressure in rats and may represent an endothelium-derived hypotensive factor.
Recent studies have also suggested that activation of CB[SUB]1[/SUB] receptors in human and rodent cardiomyocytes,^[25]^[26] coronary artery endothelial and inflammatory cells^[27]^[28]^[29]^[30] promotes activation of mitogen-activated protein (MAP) kinases p38 and JNK, reactive oxygen species generation, cell death, and cardiovascular inflammatory response both in vitro, as well as in models of heart failure, atherosclerosis and vascular inflammation.^[25]^[26]^[27]^[29]^[30]
\n\n\tPain[SIZE=small][edit][/SIZE]\t Anandamide attenuates the early phase or the late phase of pain behavior produced by formalin-induced chemical damage. This effect is produced by interaction with CB[SUB]1[/SUB] (or CB[SUB]1[/SUB]-like) receptors, located on peripheral endings of sensory neuronsinvolved in pain transmission. Palmitylethanolamide, which like anandamide is present in the skin, also exhibits peripheral antinociceptive activity during the late phase of pain behavior. Palmitylethanolamide, however does not bind to either CB[SUB]1[/SUB] or CB[SUB]2[/SUB]. Its analgesic activity is blocked by the substance that was once thought to be a specific CB[SUB]2[/SUB] antagonist, SR 144528, though not by the specific CB[SUB]1[/SUB] antagonist SR 141716A (rimonabant). Hence, a CB[SUB]2[/SUB]-like receptor was postulated.
In experiments on mice, a chemical designated JZL184 that inhibits a naturally occurring enzyme MAGL from degrading a pain-relieving endocannabinoid called 2-arachidonoylglycerol (AG) increases the brain concentration of AG, thereby inducinganalgesia.^[31]^[32]
\n\n\tBone[SIZE=small][edit][/SIZE]\t The endocannabinoid system through CB[SUB]2[/SUB] signaling plays a key role in the maintenance of bone mass. CB[SUB]2[/SUB] is expressed in osteoblasts, osteocytes, and osteoclasts. CB[SUB]2[/SUB] agonists enhance endocortical osteoblast number and activity while restraining trabecular osteoclastogenesis. Another important effect is that CB[SUB]2[/SUB] agonists attenuates ovariectomy-induced bone loss while increasing cortical thickness. These findings suggest CB[SUB]2[/SUB] offers a potential molecular target for the diagnosis and treatment of osteoporosis.^[33]
\n\n\tCannabinoid treatments[SIZE=small][edit][/SIZE]\t Main article: Medical cannabis
Cannabis preparations have been known as therapeutic agents against various diseases for millennia.^[34] The psychoactive compound tetrahydrocannabinol (THC) was found to be the principal mediator of the effects of cannabis.^[35] Synthetic THC is prescribed today, under the INN dronabinol or the brand name Marinol, to treat vomiting and for enhancement of appetite, mainly in AIDS patients.
Several synthetic cannabinoids have been shown to bind to the CB[SUB]2[/SUB] receptor with a higher affinity than to the CB[SUB]1[/SUB] receptor.^[36] Most of these compounds exhibit only modest selectivity. One of the described compounds, a classical THC-type cannabinoid, L-759,656, in which the phenolic group is blocked as a methyl ether, has a CB[SUB]1[/SUB]/CB[SUB]2[/SUB] binding ratio > 1000.^[37] The pharmacology of these agonists has yet to be described.
Certain tumors, especially gliomas, express CB[SUB]2[/SUB] receptors. Guzman and coworkers have shown that Δ⁹-tetrahydrocannabinol and WIN-55,212-2, two non-selective cannabinoid agonists, induce the regression or eradication of malignant brain tumors in rats and mice.^[38] CB[SUB]2[/SUB] selective agonists are effective in the treatment of pain, various inflammatory diseases in different animal models,^[33]^[39] osteoporosis^[33] and atherosclerosis.^[40] CB[SUB]1[/SUB] selective antagonists have previously been used for weight reduction and smoking cessation (see Rimonabant). Activation of CB[SUB]1[/SUB] provides neuroprotection after brain injury.^[41]
Several studies, using animal models, have concluded that HU210 which is a cannabinoid 100 to 800 times more potent than marijuana compounds might have the ability to prevent Alzheimer's disease.^[42]^[43] But a more recent study using mice carrying human genetic mutations that cause Alzheimer's disease found that those same cannabinoides have no effect on Alzheimer's disease and have negative consequences for cognitive function, including causing brain cell death.^[44]
\t Alot of teachers tell their students to avoid using Wikipedia to research essay's and reports ect.  because you wouldn't learn how to find your own research which is obviously very important when it comes to learning how to write a good essay, but this doesn't mean Wikipedia should be ignored the people who contribute to an encyclopedia even if its public must be nerds, and i think in general listening to what smart people have to say could never be a bad thing.
 
Thanks to Wikipedia for making me and other readers a little smarter!