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the psychopharmacology of phenethylamine

ebola?

ebola?

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hi...I was wondering how much we know about what this neurotransmitter actually does. I have seen some popular new articles that link the presence of this neurotransmitter to the induction of "love"...but these types of articles are obviously muddy and inadequate....from these correlations, we obviously cannot infer the causal role of this "trace" neurotransmitter.

have we done the studies where rats are injected with this material intercranially? As both a vegan and a cognitive scientist (okay...I'll stop being pretentious...I'm an RA for some prof.), I am ambivilant about these types of studies, but I still find them quite interesting.

ebola
 
I think any assertion of phenetylamine as a neurotransmitter are premature at best. It exsists in the brain, sure, but so do many other amines. It has an amphetamine like effect because it is a substrate for the NET and DAT, and it also an MAO inhibitor. But of course, these effect are only acheived at concentrations many orders highers than found naturally. There are a collection of G-protein coupled receptors which phenethylamine binds to with a relavent affinity, the so called "trace-amine" receptors. I don't know much about them, and I don't think anyone else does either, but it's probably something we will hear a lot more about in the future, in regards to antidepressants and recreatioanl drugs probably.

Mammalian central nervous system trace amines. Pharmacologic amphetamines, physiologic neuromodulators.
Berry MD.
J Neurochem. 2004 Jul;90(2):257-71.


The presence of the so-called trace amines 2-phenylethylamine, m-tyramine, p-tyramine, m-octopamine, p-octopamine and tryptamine in the mammalian central nervous system has been known for several decades. Despite much initial interest, these amines have largely been thought of as little more than metabolic by-products. The recent description of a family of mammalian trace amine receptors has, however, seen a resurgence of interest in the physiological role of this class of compounds. Although the trace amines are well documented to cause amphetamine-like effects, such responses only occur at concentrations multiple orders of magnitude above normal physiological levels. As such, it seems unlikely that these responses reflect the true physiological role of the trace amines. In this article previous studies showing responses to physiologically relevant concentrations of trace amines are reviewed, along with those showing a reciprocal relationship between trace amine levels and fluctuations in basal monoaminergic tone. On the basis of these studies it is hypothesized that the trace amines function as endogenous neuromodulators of classical monoamine neurotransmitters. These effects are seen as an altered neuronal sensitivity to monoamine neurotransmitters, with no change in neuronal excitability in the absence of neurotransmitter.
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Another paper which might interest you is Dopamine transporter-dependent and independent actions of trace amine beta-phenylethylamine.
 
Stuff about PEA has been around for some time, but in vague ways.

In Pikhal, Shulgin mentions that a gram and a half does nothing much, but I wondered if anyone had or knew of anyone who had used PEA in conjunction with an MAOI? What were the effects? JUst stimu;lation or any psychedelia?
 
^^ what he said. Think what happens when someone takes tyramine and MAOIs.
 
I think chocoloate might increase the amount of PEA in the brain, but perhaps this is serotonin.
 
Does phenylethylamine act as an
endogenous amphetamine in some patients?
by
Janssen PA, Leysen JE, Megens AA, Awouters FH.
Centre for Molecular Design,
Janssen Research Foundation,
B-2340 Beerse, Belgium.
Int J Neuropsychopharmcol 1999 Sep; 2(3):229-240

In brain capillary endothelium and catecholaminergic terminals a single decarboxylation step effected by aromatic amino-acid decarboxylase converts phenylalanine to phenylethylamine, at a rate comparable to that of the central synthesis of dopamine. Phenylethylamine, however, is not stored in intra-neuronal vesicles and is rapidly degraded by monoamine oxidase-B. Despite its short half-life, phenylethylamine attracts attention as an endogenous amphetamine since it can potentiate catecholaminergic neurotransmission and induce striatal hyperreactivity. Subnormal phenylethylamine levels have been linked to disorders such as attention deficit and depression; the use of selegiline (Deprenyl) in Parkinson's disease may conceivably favour recovery from deficient dopaminergic neurotransmission by a monoamine oxidase-B inhibitory action that increases central phenylethylamine. Excess phenylethylamine has been invoked particularly in paranoid schizophrenia, in which it is thought to act as an endogenous amphetamine and, therefore, would be antagonized by neuroleptics. The importance of phenylethylamine in mental disorders is far from fully elucidated but the evolution of phenylethylamine concentrations in relation to symptoms remains a worthwhile investigation for individual psychotic patients
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Sustained antidepressant
effect of PEA replacement
by
Sabelli H; Fink P; Fawcett J; Tom C
Rush University and the Center for
Creative Development, Chicago, Illinois, USA.
J Neuropsychiatry Clin Neurosci, 1996 Spr, 8:2, 168-71

Phenylethylamine (PEA), an endogenous neuroamine, increases attention and activity in animals and has been shown to relieve depression in 60% of depressed patients. It has been proposed that PEA deficit may be the cause of a common form of depressive illness. Fourteen patients with major depressive episodes that responded to PEA treatment (10-60 mg orally per day, with 10 mg/day selegiline to prevent rapid PEA destruction) were reexamined 20 to 50 weeks later. The antidepressant response had been maintained in 12 patients. Effective dosage did not change with time. There were no apparent side effects. PEA produces sustained relief of depression in a significant number of patients, including some unresponsive to the standard treatments. PEA improves mood as rapidly as amphetamine but does not produce tolerance.
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Interesting that they didn't get bad side effects... but that 2nd study is shit-house. A) not placebo controled, just giving depressed patients placebos produces noticable antidepressant effects b) MAOIs are antidepressant, and despite what people tell you, MAO-BIs are antidepressant as well.
 
Shame, could you imagine getting a prescription for chocolate?! (Pharmacist: There's yor selegeline tablets, and there's your quater kilo of Suchard chocolate squares (noise a la Homer Simpson) Patient: Help, I think I've overdosed!)
 
fastandbulbous said:
Shame, could you imagine getting a prescription for chocolate?! (Pharmacist: There's yor selegeline tablets, and there's your quater kilo of Suchard chocolate squares (noise a la Homer Simpson) Patient: Help, I think I've overdosed!)
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There's been a few articles in newspapers here in the UK about medical choc' and I've also read I think it was at www.chocolate.org or some where else that some company is looking into 'medical grade' chocolate with certain chem's in it increased. :\
 
^ My wife attended a conference in Germany, and brought me back some chocolate that she thought I might like (like there's chocolate I don't like!), and we both discovered that 3-4 squares of each of these chocolates produced a mild opiate/stimulant like effect that lasted about half an hour (like a massively enhanced feeling of strong coffee after a hot spicey meal). I've tried it with a couple of friends, and they've noticed it as well.

I know it can be ordered from some site on the internet, but next time we/she goes to Germany, Im bringing back a couple of boxes. Eaten after a nice meal, it makes for a wonderful 'drug-free' evening.

I scanned the wrappers in, and they're in the attached jpeg
 
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BilZ0r said:
Interesting that they didn't get bad side effects... but that 2nd study is shit-house. A) not placebo controled, just giving depressed patients placebos produces noticable antidepressant effects b) MAOIs are antidepressant, and despite what people tell you, MAO-BIs are antidepressant as well.
Click to expand...

The placebo response isn't generally that large though... Why do you think MAO-Bs are antidepressants? Because they produce a dopamine rise? PEA related? Or because there's some impact on 5-HT/NE?
 
No, the placebo effect is almost the same as the antidepressant effect. When you use active placebos, so you don't get unblinding, the "effect" of a lot of antidepressants can no longer be demonstrated.

I think MAO-BIs are antidepressant because the research is there to back it up, like this.. the animal data is there too...
 
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