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Scientific Research on Phenylethylamine
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β-phenylethylamine (2-phenylethylamine) is a small amine containing alkaloid synonymous with phenethylamine and the acronym PEA; in the human body it has a neurotransmitter role and is known as a trace amine due to its low quantity relative to other bioactive amino acids.
Structurally speaking, the basic phenethylamine backbone (2-phenylethylamine) contains a benzene ring with a lone nitrogen group bound via a short two-carbon chain; if a methylation were to occur at the final carbon that is attached to the nitrogen group then the resulting backbone is the base amphetamine structure. The phenylethylamine backbone differs from catecholamines due to having no hydroxylations on its backbone, and synthetic modifications of the backbone with hydroxylations and methylation results in a variety of phenylethylamine-based hallucinogenic drugs (ie. mescaline).
It can be found naturally occurring as an endogenous amine in various algae and bacteria, and similar to alkaloids such as tyramine, octopamine, and hordenine it is seen as a biogenic amine. It can be found in natto secondary to the bacteria used to ferment it, and has also been detected in eggs as well as chocolate where it is produced during thermal decomposition of L-phenylalanine (it's parent amino acid).
β-phenylethylamine can also be produced from dietary L-phenylalanine which is estimated to be around 4g in the average diet (due to it being a component of dietary protein), although not all L-phenylalanine is destined to produce β-phenylethylamine as it can be converted into L-Tyrosine via phenylalanine hydroxylase.
β-phenylethylamine has a molar mass of 121.17964 g/mol and has high solubility in double distilled water (ddH2O) and in plasma, although low solubility in lipid.
β-phenylethylamine is produced from L-phenylalanine, which is also known to by converted into L-Tyrosine via the phenylalanine hydroxylase enzyme. Chronic inhibition of this enzyme or genetic insufficiency results in a backlog of L-phenylalanine, resulting in a form of hyperphenylalaninemia and is involved in some cases of phenylketonuria (PKU). Persons in this situation tend to be more sensitive to most biogenic amines including β-phenylethylamine.
R-β-Methylphenylethylamine (1-amino-2-phenylpropane), also known simply as β-Methylphenethylamine or β-Me-PEA, is a PEA structure where a methyl group occurs on the first carbon extending out from the benzene backbone; due to the carbon being placed here rather than the second carbon out, it is not classified as an amphetamine and has been isolated from the leaves of acacia berlandieri (Guajillo; not the pepper).
N-Methylphenethylamine (NMPEA; N-Methyl-β-phenylethylamine) is a differently structured metabolite of PEA where the methylation occurs on the amine itself, and NMPEA is also not classified as an amphetamine.
There are two variations of the basic phenylethylamine structure involving methylation, but neither of which are methylated on the second carbon (which would be an amphetamine); one methylates on the first carbon from the benzene ring whereas the other directly methylates the amine group
A collection of intracellular receptors known as trace amine-associated receptors (TAARs) or simply trace amine (TA) receptors are known to respond to the variety of amino acids known as trace amines. These receptors are known to be expressed in both rats and humans although their response to drugs may differ due to somewhat low homology (76–78%) although recombinant human TAARs (rhTAAR) and human TAAR (hTAAR) have high homology (96.9%). These receptors are intracellular and associated with the membrane fraction of cells excluding the cell surface membrane despite their similarities to adrenergic receptors (which are at the cell surface membrane), thought to be due to the nine-amino acid long proximal terminal of adrenergic receptors which, when added to TAAR1, can stabilize it in the cell surface membrane.
Trace amine receptors are intracellular receptors which respond to the neurotransmitters that are in lower amounts without their own receptors. These neurotransmitters include tyramine, tryptamine, octopamine, β-phenylethylamine, and 3-Iodothyronamine amongst others, and this signalling pathway highly interacts with catecholamine (dopamine, adrenaline, noradrenaline) signalling
The TA1 receptor (also known as TAAR1) is a G-protein coupled receptor with structural hallmarks that parallel the rhodopsin/β-adrenergic receptor superfamily that responds to trace amines including tyramine and β-phenylethylamine, and after binding produces cAMP. TA2 (aka. GPR58 or TAAR2) is a similar receptor that also responds to β-phenylethylamine but instead of tyramine it responds to tryptamine, and both the TA1 and TA2 receptors have mRNA expressed in brain regions (substantia nigra/ventral tegmental area, locus coeruleus, and dorsal raphe nucleus) where β-phenylethylamine is known to exert catecholaminergic activity.
This receptor (TA1) is known to have a baseline activity without any ligand, and β-phenylethylamine is more potent than other TA1 agonists (tyramine and octopamine) at inducing cAMP a concentration of 1µM (but comparable at 100nM or less).
β-phenylethylamine is an endogenous agonist at the TA1 and TA2 receptors, with slightly more potency than other trace amines. Actions at this receptor are thought to explain the roles of β-phenylethylamine in interacting with adrenergic and dopaminergic neurotransmission
Secondary to the activation of TA1 (previous section) β-phenylethylamine has been noted to both reduce the uptake of and increase efflux of various neurotransmitters such as dopamine, serotonin, and noradrenaline in brain synaptosomes at 0.1-1μM (no activity at 10nM); this did not occur in cells where TA1 was genetically ablated, was unrelated to autoreceptor function (which regulate receptor function) and the efflux was blocked by inhibiting the transporters.
β-phenylethylamine (PEA) is a naturally occurring biogenic amine in the mammalian brain although it is considered trace as its overall amount totals around 1-5% of the level of catecholamines, thought to be due to limited synthesis with rapid metabolism. Injections of β-phenylethylamine in the periphery seem to be taken up in most brain areas evenly, and at rest β-phenylethylamine seems to be spread across most brain regions although highest levels are in areas with a higher catecholamine presence (nigrostriatal and mesolimbic regions such as the caudate–putamen, olfactory tubercles and nucleus accumbens).
β-phenylethylamine appears to cross the blood brain barrier after arterial injection showing a brain uptake index of 83+/-6% (water as reference at 100%) comparable to amphetamine and suggesting passive diffusion rather than transporter-mediated uptake.
Within the brain (not serum), β-phenylethylamine is estimated to have a half-life of around half a minute due to rapid metabolism by MAO enzymes (primarily MAO-B).
β-phenylethylamine (PEA) is primarily metabolized by the monoamine oxidase B enzyme (MAO-B) although both enzymes have the potential to metabolize it. This deamination process by MAO enzymes results in production of the byproduct phenylacetic acid and at least neurologically it does not appear to be active in the same way β-phenylethylamine is.
Based on studies injecting β-phenylethylamine into the dog, the half-life of PEA appeared to be in the range of 6-16 minutes depending on dose and N-methyl-β-phenylethylamine (NMPEA) appears to follow suit in this rapid metabolism and is also a known substrate for MAO-B.
β-phenylethylamine appears to be primarily metabolized by MAO-B, and this metabolism appears to occur quite rapidly in serum
Interconversions may also happen in cells, as nonspecific N-methyltransferase enzymes can convert β-phenylethylamine into N-Methylphenethylamine (NMPEA) and dopamine-β-hydroxylase can convert PEA into a phenylethanolamine (PEOH); PEOH can be further methylated by the specific enzyme phenylethanolamine N-methyltransferase (PNMT) which is the enzyme that converts noradrenaline into adrenaline. It should be noted that PEOH is also a substrate for both MAO enzymes with specificity for MAO-B.
β-phenylethylamine produced in neurons (from L-phenylalanine) can be used by alternate enzymes as an intermediate in a few pathways involved in neurotransmission
Catecholaminergic neurons tend to express a high level of aromatic amino acid decarboxylase (AADC) which produces β-phenylethylamine (PEA) from its parent amino acid L-phenylalanine, while the enzyme of metabolism (MAO-B) tends to be expressed in high levels in astrocytes but there was a failure to express high levels of MAO-B in catecholaminrgic neurons (locus coeruleus and substantia nigra) despite detecting MAO-B in serotonergic neurons. This has been interpreted as a potential higher concentration of PEA within catecholaminergic neurons than is generally assumed based on assessing brain wet weight.
The enzymes of β-phenylethylamine synthesis are located alongside those of catecholamine synthesis, and due to a relatively lower amount of its enzyme of metabolism in cells that have a high noradrenergic presence it is thought to accumulate to a degree and be more intracellularly active in these brain regions
At the level of the adrenergic receptor, β-phenylethylamine (and tyramine) are partial allosteric antagonists of both the β1 and β2 (noncompetitive against the agonist isoprenaline) with an Emax of 403+/-54nM.
PEA is thought to be an antagonist at the α-adrenergic receptor albeit at impractically high concentrations (100µM).
At the level of the adrenergic receptors, β-phenylethylamine appears to be an allosteric and partial inhibitor
β-phenylethylamine synthesis rates in dopaminergic neurons parallel that of dopamine, although striatal concentrations seem to be about 3-fold lower due to elevated MAO-B metabolism.
β-phenylethylamine appears to be localized around dopaminergic neurons, although it is at a lower concentration than dopamine due to its rapid metabolism by MAO-B
β-phenylethylamine has been noted to increase dopamine secretion when taken up into dopaminergic neurons, secondary to the dopamine transporter (DAT; as blocking the transporter ablates the effects of PEA); the vesicular monoamine transporter not playing a role in vitro and the VMAT inhibitor reserpine not blocking the dopaminergic actions of β-phenylethylamine. This may be due to β-phenylethylamine being a substrate for DAT, and increasing dopamine secretion secondary to TA1 activation. Similar to the actions expected of a TA1 agonist, β-phenylethylamine has been repeatedly shown to induce dopamine secretion in vitro and in vivo and to inhibit dopamine uptake.
Secondary to activation of the trace amine receptor (TA1), β-phenylethylamine appears to cause an increase in dopamine efflux paired with a reduction in dopamine uptake into neurons
β-phenylethylamine appears to be 100-fold less potent in releasing serotonin from the nuclear accumbens when compared to its ability to release dopamine when tested in the range of 1-100µM.
β-phenylethylamine is thought to be related to addiction since, in the treatment of cocaine addiction, 'agonist therapy' (using agents that increase synaptic dopamine) appear to be beneficial but pure dopaminergic agonists have their own addictive potential due to activation of the mesolimbic reward pathway. As serotonin suppresses this particular aspect of dopaminergic activity, mixed agonists acting on both serotonin and dopamine are thought to be beneficial for the treatment of stimulant and alcohol addiction; β-phenylethylamine is known to possess agonistic properties towards both of these neurotransmitters.
In subjects exercising on a treadmill for half an hour at 70% of their maximal heart rate (in the middle of the 60-80% range where increases in mood are reported) the amount of phenylacetic acid in the urine was increased albeit to a highly variable degree; this was thought to be a possible factor in the anti-depressant actions of exercise.
The trace amine receptors that β-phenylethylamine is known to influence (TAAR1 and 2) appear to be expressed on leukocytes as well as both T and B cells, and activation of both receptors by β-phenylethylamine at an EC50 of 0.52+/-0.05nM causes chemotaxis of the immune cells; this is a concentration already lower than human plasma at rest (14.5nM) and thus appears to be physiologically relevant. Similar actions were also noted with the trace amines T1AM (3-Monoiodothyronamine, EC50 0.25+/-0.04nM) and tyramine (0.52+/-0.05 nM) which are also within physiological concentrations.
Trace amino acids appear to be able to influence leukocyte migration at a concentration which is relevant even without nutritional supplementation
TAAR1 and TAAR2 do not appear to be highly expressed in natural killer cells.
Trace amines, including octopamine and p-tyramine (59% inhibition at 1µM, some efficacy at 10nM) as well as phenylethylamine can inhibit prolactin secretion. The inhibitory effects of phenylethylamine are dose-dependent in the range of 10nM upwards to 10µM, and while this effect requires dopamine receptors to be functioning trace amines do not displace dopamine receptor ligands at this concentration. It is thought that trace amines cause a secretion of dopamine which then acts on its receptors to reduce prolactin (a known phenomena).
Parkinson's Disease (PD) is pathologically characterized by dopaminergic insufficiency and degeneration in the brain region known as the substantia nigra, resulting in a loss of function in the nigrostriatal pathway and dopamine content of the caudate-putamen. The nigrostriatal pathway locally synthesizes and is modulated by trace amines such as β-phenylethylamine.
One study noted a negative correlation between cerebrospinal fluid content of β-phenylethylamine and the severity of Parkinson's disease as assessed by Hoehn and Yahr stage although a later study assessing serum β-phenylethylamine failed to replicate this correlation with disease severity although PD per se had a significantly lower serum level of this trace amine (48%).
β-phenylethylamine is synthesized in and acts on the brain region which is known to dysfunction during Parkinson's disease, and accordingly concentrations of β-phenylethylamine in the blood and cerebrospinal fluid appear to be reduced during Parkinson's Disease
β-phenylethylamine (PEA) is metabolized by monoamine oxidase B (MAO-B), and inhibiting these enzymes in the presence of PEA has been noted to cause effects attributed to PEA that did not otherwise occur without inhibition of its metabolism.
A condition known as 'cheese syndrome' or the 'cheese effect' is known to occur with high intake of cheese (conferring dietary tyramine) and chocolate (conferring dietary β-phenylethylamine) in persons who are using MAO inhibitors, where the combination results in a potentially dangerous increase in blood pressure. It appears that selective inhibition of MAO-B is not a risk, but selective inhibition of MAO-A and mixed inhibition is.
Mechanistically, β-phenylethylamine has been suggested to potentiate amphetamine-like actions in a manner not related to endogenous noradrenaline.
As amphetamine is known to rapidly increase dopamine transporter trafficking to the cell surface (although afterwards promoting receptor internalization) and the effects of β-phenylethylamine on dopamine secretion depend on this transporter, it is thought to be a possible level for interaction and may preclude long term synergism (as the increased DAT expression does not last after one hour).
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