Author Topic: Pharmacology of PEA's, mechanism of action.  (Read 347 times)

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Offline Thetakishi

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Pharmacology of PEA's, mechanism of action.
« on: September 09, 2014, 12:56:24 am »
Originally posted by Psychomanthis aka Iudicium Infernalum

Foreword

This is for all you out there that, like me are not only interested in drugs because they get you high, but are interested in how a substance alters our neurochemistry which in turn affects what we percieve and feel.

I have chosen phenyletheylamines (The 2c family to be exact) as my subject of research frankly because this, in my opinion, is a amazing group of substances with effects unlike any of the other psychoactive drugs i have had the privilege to sample.



Analysis

Let me start by saying i have tried 2c-B, 25c-NBOMe, 2c-I 2c-D and 25d-NBOMe. From these i found 2c-D the most enjoyable "high" and 25c-NBOMe the most expressive in terms of hallucinogenic effects (Remember that this is all from personal experience). I will compare these two in my analysis because i believe they have distinctive differences in their respective mechanisms of action which presents itself in the effects percieved. I will go into detail in the paragraphs below.

This is how i break it down for 2c-D
After 2c-D has broken through the BBB it functions as an antagonist of the 5-HT2C serotonin recpetor. This receptor is responsible for regulating mood and anxiety among others. It works in a different way though then you would expect. From wikipedia:
Quote:
5-HT2C receptors mediate the release and increase of extracellular dopamine in response to many drugs,[9][10] including caffeine, nicotine, amphetamine, morphine, cocaine, and others. 5-HT2C antagonism increases dopamine release in response to reinforcing drugs, and many dopaminergic stimuli. Feeding, social interaction, and sexual activity all release dopamine subject to inhibition by 5-HT2C. Increased 5-HT2C expression reduces dopamine release in both the presence and absence of stimuli.

Link 

This led me to believe that 2c-D works in a similair way; antagonising 5-HT2C thus increasing levels of dopamine and as you can read in the article i linked to nor-epinephrine. Which would explain the feeling of being stimulated that some users of the 2c family report (Including myself) when under the influence of some if not all drugs of this kind. 

5-HT2A agonism 
As some of you might be aware, all classic hallucinogenics are either full or partial agonists of the 5-HT2A serotonin receptor. Which produces effects like CEV's, OEV's, euphoria, general sensory hallucinations and general mood elevation. I theorise that most of the 2c family are partial agonists of the 5-HT2A receptor but are less potent in this respect when compared to substances like LSD. Which would account for the reasonably mild hallucinogenic qualities of these phenylethylamines.

2c-D and 25c-NBOMe 
This leads me to my comparison of the effects of 2c-D and 25c-NBOMe. I believe that 2c-D is a less effective agonist of the 5-HT2A receptor and a potent antagonist of the 5-HT2C receptor. Which accounts for what i percieved as more stimulation and less hallucination while on it. I believe that the same is true for 25c-NBOMe but in reverse. With 25c' being a much more potent 5-HT2A agonist and a less potent antagonist of the 5-HT2C receptor. Giving it it's quality of being more hallucinogenic and less "stimulating".



Conclusion

I believe different effects percieved when under the influence of any PEA of the 2c family are closely related to how these receptors act and interact. With varying affinity to the receptors i described respective of the different constituents of the 2c family.


Thank you for reading i hope you found my analysis interesting and would love to hear your thoughts about this subject!

Links to the articles i am basing this on:

Pharmacology of 2cB
5-HT2C Receptor 
5-HT2A Receptor