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PEA: In absense of MAO, DARI or Releaser?

Ham-milton

Ham-milton

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Jul 20, 2007
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I was wondering if anyone could point me to a study that looked at PEAs effect sans MAO. With the spreading availability of internet obtained selegiline, it might be worth knowing (I've considered giving it a shot recently, actually).

I'm standing here nekkid about to shower.

Ladies, feel free to ogle.
 
Oh wait, this isn't SLR (and we're dealing with a hard science) there are no ladies here, silly me.

Well fella's.... Don't let that stop you. Murphy, above the waist please ;)

Actually I got in trouble there the other day for posting an infamous midget porn picture in SLR that (I believe) a lady who used to post frequently posted (obviously at blacklight- where the chem pervs hang out, I guess).
 
Ham-milton said:
Oh wait, this isn't SLR (and we're dealing with a hard science) there are no ladies here, silly me.

Well fella's.... Don't let that stop you.
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Nice amine tail, hammy.
 
Thanks, I think it'd more properly be called an amIDE, though, for obvious reasons.
 
samadhi_smiles said:
do you have studies?
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I don't expect someone with any medical knowledge to understand. Any compound given at a high enough dose will saturate it's breakdown enzyme and levels will increase.

In my clinical experience I have currently 54 people on PEA all of the reporting clear psychoactive effects at various doses.

Do you have any basis for why PEA would not reach the brain if give at a high enough dose? I would easily compare it to DMT in terms of breakdown.
 
DMT has been administered orally at dosage levels many times the active dose and still does not get past MAO.

Shulgin in TIHKAL said:
(with 350 mg, orally) "Completely without effect either physiological or psychological."
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Ott tried a 2 gram dose I believe but I can't find the reference.
 
samadhi_smiles said:
DMT has been administered orally at dosage levels many times the active dose and still does not get past MAO.

Ott tried a 2 gram dose I believe but I can't find the reference.
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Obviously they did not use a high enough dose. Or the proper dosing as I have posted for everyone benefits.
 
NeuronalPerception said:
DMT normally should not reach the BBB in small amounts due to MAO-B breakdown, however when smoked in the right amount it by passes most MAO-B and reaches the brain where it is broken down within 30 mins. If enough of a oral dose or an MAO-B inhibitor were take it would work. Same as PEA.
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DMT is eaten up by MAO-A
 
Thanks Phrozen. Is there actually any evidence that even in massive doses PEA can get through enough to have any effect? I can't find any studies supporting that claim.
 
It's action appears to be similar to amphetamine, causing the DAT to funnel dopamine backwards into the cleft while at the same time releasing dopamine, etc. Obviously it has affinities for the trace amine receptors that amphetamine does not have, so because of this PEA might have a somewhat more complex pharmacology. I am not sure what the role of the trace amine receptor is, although I had read about the link to schizophrenia.


Abstract. Rationale and objective: Sufficiently high doses of β-phenylethylamine (β-PEA), a trace amine that is rapidly metabolized by monoamine oxidase-type B (MAO-B), can produce effects comparable to those of cocaine or methamphetamine (MA). The present experiments were conducted to study how the discriminative-stimulus (SD) and reinforcing-stimulus (SR) effects of β-PEA in monkeys are modified by treatment with inhibitors of MAO-B [R-(–)-deprenyl and MDL 72974]. Methods and results: In studies of its SD effects, doses of β-PEA up to 30 mg/kg engendered only sporadic responding on the drug-associated lever in squirrel monkeys that discriminated intramuscular injections of 0.3 mg/kg MA from vehicle whereas lower doses of 0.3–1.0 mg/kg β-PEA produced full substitution when administered after either R-(–)-deprenyl or MDL 72974 (0.3 mg/kg). The MA-like SD effects of β-PEA were attenuated by either dopamine D1 or D2 receptor blockers. In studies of its SR effects, high doses of β-PEA maintained responding in two of three monkeys under a second-order fixed-interval schedule (3.0 or 10 mg/kg per injection) and two of three monkeys under a simple fixed ratio (FR) schedule (0.3–1.0 mg/kg per injection) of intravenous (i.v.) self-administration. MAO-B inhibition by R-(–)-deprenyl or MDL 72974 enhanced the SR effects of β-PEA in all monkeys and, under the FR schedule, induced a 30-fold or greater leftward shift in the dose-response function for its i.v. self-administration. Based on time-course determinations, the enhanced SR effects of β-PEA under the FR schedule were long-lasting and dissipated gradually over 3–7 days. Conclusions: These results show that inhibition of MAO-B enhances SD and SR effects of β-PEA in monkeys, presumably by delaying its inactivation. MAO-B inhibition leading to increased levels of β-PEA may be useful, alone or in combination with other therapeutic agents, in the pharmacological management of selected aspects of drug dependence.
http://www.springerlink.com/content/k5pgyfdrcp3yvw7w/
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From this it sounds like one would need quite a bit without a MAO-B, especially if 30m/kg was only sometimes effective in replacing methamphetamine...


Didn't someone post a thread in ADD where they claimed to have tried 50mg of PEA intravenously? Oh wait, that was the guy who said he performed a synthesis of 2-AG over a campfire....
 
here's this:
Shulgin in PIHKAL said:
DOSAGE: greater than 1600 mg.

DURATION: unknown.

QUALITATIVE COMMENTS: (with 200, 400, 800 and 1600 mg) No effects.

(with 500 mg) No effects.

(with 800 and 1600 mg) No effects.

(with 25 and 50 mg i.v.) No effects.

EXTENSIONS AND COMMENTARY: Here is the chemical that is central to this entire book. This is the structural point of departure for every compound that is discussed here. It is the RPS in PIHKAL. It is without activity in man! Certainly not for the lack of trying, as some of the dosage trials that are tucked away in the literature (as abstracted in the "Qualitative Comments" given above) are pretty heavy duty. Actually, I truly doubt that all of the experimenters used exactly that phrase, "No effects," but it is patently obvious that no effects were found. It happened to be the phrase I had used in my own notes.
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This leads me to suggest that we're not dealing with the task of simply 'saturating' MAO-B in the liver, but rather the chemical doesn't cross the BBB.
 
It seems unlikely to me that it's not crossing the BBB, since every indication seems to be that, with MAO inhibition it produces very amphetamine-y effects.
 
I think it is lipophilic enough to pass by the BBB--after all, it is just one methyl group away from amphetamine, with no polar ring substituents to impede its passage into the brain. I estimate that two factors prevent it from being particularly active without an MAOI: (1) it takes a shitload to effectively inhibit MAO-B, as the monoamine oxidase enzymes have fast kinetics and (2) MAO-B is simply the preferred metabolic target, in the wake of super-high gut phenethylamine concentrations, I'm sure MAO-A picks up the slack. There are also plenty of MAOs in the brain, which is why DMT is extremely short-acting when administered IV.

So I think we can safely close the book on this one and say that it is virtually inactive without activation, just like DMT (but with a different preferential metabolic enzyme). With some (l)-deprenyl, it might actually really enjoyable. My experience with (l)-deprenyl and (D)-phenylalanine certainly wasn't bad, not quite as good as amphetamine proper, but no bad.
 
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