In 1988, scientists located the body's receptors for THC -- the chemical responsible for the psychological and physical effects of marijuana. Two types of receptors were found: the CB1 in the central nervous system, and the CB2 located in various other parts of the body, notably the uterine wall and the lungs. Of course, the body doesn't tend to have receptors for chemicals it doesn't produce, so the search was on for a natural ligand of the cannabinoid receptors, an endocannabinoid. It was finally found in 1992 by Dr. Raphael Mechoulam of Israel, the same researcher who had isolated THC from marijuana almost thirty years earlier. The chemical's name was N-arachidonoylethanolamine, but Mechoulam called it anandamide, from the Sanskrit word for eternal bliss.

One of anandamide's roles in the CNS is in the area responsible for short term memory. Weed's deserved reputation for disruption of short term memory comes from its activity at these sites. Memories are formed (at least in part) through by the action of long term potentiation. This occurs when a group of neurons is consistently fired synchronously, they tend to become quicker to fire together, and their response is stronger -- they are associated with each other, and are a memory. If these groups are not stimulated together for a long period of time, their potentiation goes away, and you forget whatever memory they held. CB1 agonism, whether done by anandamide or THC, indirectly causes the neuron's ion gates to open, forcing the neuron to go to resting potential whether or not it is supposed to be firing. Since the neuron's firing is inhibited, long term potentiation involving that neuron is prevented. When caused by anandamide (in its role as a neurotransmitter), this effect is used in specific areas to the brain's benefit. THC is nonspecific, so all short term memory is impaired, and THC is much longer lived than anandamide, making it's effects last longer. There have been a few studies that suggest blocking the CB1 receptor can lead to improved memory in both healthy and aging rats, and drugs are being studded to use this effect for humans.

Another nervous system function of Anandamide is to regulate dopamine release in the brain's movement centers, keeping it from becoming too strong. It is produced by neurons that are being stimulated by dopamine, and binds to surrounding CB1 receptors, providing negative control on movement. Theory suggests that diseases caused by an excess of dopamine (or oversensitive dopamine receptors) such as Tourette's syndrome and schizophrenia might be treatable with drugs that upregulate or mimic anandamide. This might be the reason that schizophrenia sufferers are twice as likely to begin smoking grass as healthy adults. Diseases caused by too little dopamine, like Parkinson's, might also be treatable with an anandamide blocker of some kind. Incedentaly, the CB1 receptor's interactions with dopamine are what make a few bong hits able to take the edge off of a cocaine high.

CB2 receptors are found in the uterine wall, and play an important role in pregnancy. CB2 receptors are about 100 times as common here as CB1 receptors are in the brain, and concentrations are just as high in a developing embryo. Anandamide provides synchronization between the embryo and the uterus, slowing down the embryo's development until the uterine wall is able to be implanted upon. It may also take part in embryo selection, determining if an embryo will implant -- and thus be viable -- by whether it has the right concentrations of CB2 receptors. Anandamide also prevents one embryo from implanting too close to another, as anandamide levels near an implanted embryo fall sharply. Theory suggests (but to the best of my knowledge this is untested) that cannabis use causes so much CB2 receptor activity in the uterus that the likelihood of becoming pregnant is lessened -- sort of a natural contraceptive.

There are also CB2 receptors in the lungs which control lung contraction, though their reason for being there is still unknown. In healthy lungs, addition of an anandamide agonist (such as THC) causes the bronchioles to open up and the lungs to relax. In lungs where the vagus nerve (responsible for lung muscle contraction) has been severed, CB2 activity causes the lungs to contract back to a normal state. If it's strong enough, CB2 activity can relax the lungs to the point that they no longer have a cough reflex when exposed to capsaicin, the active ingredient in pepper spray. Research on using anandamide analogs as cough medicines is ongoing, and may eventually be able to stop chronic coughing caused by disease.

Finally, this writeup wouldn't be complete unless I mentioned chocolate, even though the Anandamide-Chocolate link is tenuous at best. In every gram of processed chocolate and cocoa powder there are a few micrograms of anandamide and other fatty acids that may bind to CB1 sites. Some folks theorize that they are responsible for chocolate's comforting effect, and even peoples' craving for chocolate. This makes for good headlines, but is ultimately bullshit. Barely anything has perceptible effects in the low microgram range, and certainly not anandamide. With THC (and thus anandamide) effects start to become present in the single digit milligrams dosages.

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