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Endogenous cannabinoid signaling
1. Endogenous Cannabinoid Signaling
Various drugs of abuse have effects on our brains because they resemble the neurotransmitters that our
brains produce. For example Endorphines and Enkephalins resemble exogenous morphine or heroin,
Endogenous Anandamide resembles marijuana, acethylcholine resembles nicotine and
cocaine/amphetamines resemble dopamine, etc.
The endogenous cannabinoid signaling (ECS) is a complex endogenous signaling system comprised of
Cannabinoid receptors (CB1 and CB2), Endocannabinoid ligands, and proteins that are involved with
endocannabinoid synthesis.
To learn more:
http://www.rtbot.net/play.php?id=B6QWT-WP09o
At present, there are two known types of cannabinoid receptors, termed CB1 and CB2, with mounting
evidence of more.
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.
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
Anandamide was discovered in 1992 and is our endogenous cannabinoid. It is synthesized in the body
from N-arachidonoyl phosphatidylethanolamine by multiple pathways.
Endogenous anandamide is present at very low levels and has a very short half-life due to the action of
the enzyme fatty acid amide hydrolase (FAAH) which converts anandamide into ethanolamine and
arachidonic acid.
Inhibitors of FAAH lead to elevated anandamide levels and are being pursued for therapeutic use.
Fatty-acid amide hydrolase (FAAH) activity has been linked with arousability and aversive-memories
extinction.
Paradoxically, Anandamide may help memory by helping us forget. The brain's ability to weaken
unimportant memories and experiences enables it to function more efficiently. Just as long term
potentiation (LTP) is important for remembering, long term depression (LTD) is important for forgetting.
For this reason FAAH inhibitors are looked at in PTSD.
Learn more:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3309545/
3. Cannabidiol
Cannabidiol is a component of marijuana that does not activate cannabinoid receptors, but inhibits the
degradation of the endo cannabinoid anandamide by inhibiting FAAH. A study published May 20th, 2012
in Translational Psychiatry demonstrates that Canabidiol alleviates psychotic symptoms in schizophrenia
just like the antipsychotic medication, without causing adverse effects:
http://www.nature.com/tp/journal/v2/n3/full/tp201215a.html
This is but one of the potential applications of Cannabidiol, but there are many more:
In neurodegenerative disorders
Cannabidiol acts as an anti‐inflammatory, anticonvulsant, antioxidant, antiemetic, anxiolytic and
antipsychotic agent, and is therefore a potential medicine for the treatment of neuroinflammation,
epilepsy, oxidative injury, vomiting and nausea, anxiety and schizophrenia, respectively. The
neuroprotective potential of CBD, based on the combination of its anti‐inflammatory and antioxidant
properties, is of particular interest and is presently under intense preclinical research in numerous
neurodegenerative disorders.
