Intro to the Endocannabinoid System

in #usa9 months ago


Everyone get to know these. These can be found in plants which are completely unregulated:


The CB2 receptor is Munchies, Immuno-activator, Anti-Epilepsy, kind of like Brain grease to oil the machine.

The CB1 receptor is pretty much everything else, Psychoactive, Tumor shrinking, etc.

FAAH is what breaks down Endorphines and Endocannabinoids. So an FAAH Inhibitor stops the breakdown.

MAGL Inhibitors are kind of Esoteric. So, to understand these it is best to understand EndoCannabinoid Reuptake Inhibitors (eCRIs). This is like an FAAH Inhibitor, but specialized for the Endocannabinoids. Tylenol is the most common, it breaks down into AM404 which is an eCRI. And MAGL seems to work on another level similar to an eCRI.

Oleamide is apparently also a CB1 agonist

And it is what makes you tired when you are sleep deprived. It uses your inner Cannabinoids to make you tired.

More FAAH Inhibitors

So what the MAGL Inhibitors do is a selective Inhibitor to keep 2-AG and other Cannabinoids and Endorphins in the brain, focusing on Cannabinoids

Other enzymes including ABHD6 and ABHD12 may also involve in the metabolism of 2-AG but to a much less extent compared to MAGL.

a previous study showed that MAGL is responsible for approximate 85% of the 2-AG-hydrolyzing activity in mouse brain

MJN110 is a MAGL used in research

Another strategy to reduce the central side effects is to use positive allosteric modulators (PAMs) of CB1Rs rather than typical orthosteric agonists. Allosteric modulators are substances that bind to a receptor and change the response of the receptor by either increasing its affinity to agonists or its ability to be activated by agonists.


I am pretty sure Oxytocin is a positive Activity Modulator, they just haven't researched it in those words yet. They also say Indoles are PAMs so probably any small you would say "is your favorite smell" is probably a PAM.

Some good information is about to be coming from this website, here is my intro thread here but there is a Kava Potentiation thread on this website that is about to be groundbreaking in that personal research is being done that is beyond current understanding or any clinical studies going on. So it will add to human understanding and will be a springboard for other personal studies, clinical studies, etc.
"Morphological, chemical, cytological and genetic evidence demonstrating the absence of taxonomic distinction between Piper methysticum and Piper wichmannii are reviewed. Piper methysticum is not a separate species, but rather a group of sterile cultivars selected from somatic mutants of P. wichmannii. As P. methysticum was described first (1786), it has priority and P. wichmannii (1910) is superfluous. A new subspecific classification is suggested that makes a distinction between the sterile cultivars (P. methysticum var. methysticum) and the wild populations (P. methysticum var. Wichmannii)."


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