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PubMed2001

[Determination of enantiomeric purity of (S)-(-)-alpha-phenylethylamine by NMR].

It was reported the determination of enantiomeric purities of (S)-(-)-alpha-phenylethylamine by 1H NMR, using (2R, 3R)-dibenzoyl-tartaric acid as chiral solvating agent. 1H NMR chemical shift non-equivalence of the methyl doublet of alpha-phenylethylamine was 0.08 ppm(base-line separation) in solvent CDCl3, when the concentration of the sample was 0.051 mol.L-1, the molar ratio between chiral solvating agent and the sample was 0.33. The enantiomeric purities could be determined by the peak areas of the methyl doublet of alpha-phenylethylamine. The relative standard deviation depended upon the enantiomeric purities of sample. With enantiomeric purities as high as 99.1% ee, the RSD was 0.3% (n = 4).

Magnetic Resonance Spectroscopy↗

PubMed1979

Amphetamine- and phenylethylamine-induced alterations in dopamine synthesis regulation in rat brain striatal synaptosomes.

Amphetamine and phenylethylamine stimulate dopamine synthesis in rat brain striatal synaptosomes via a calcium- and tyrosine-dependent mechanism. The similarity of this stimulation to that produced by depolarizing concentrations of veratridine, along with the non-additivity of maximally stimulating concentrations of amphetamine and veratridine, suggests that these treatments may all share a common locus of action. Differences in exact modes of action can be seen, however, in the blockade only of the stimulation of veratridine by tetrodotoxin, and by the lack of effect of amphetamine or phenylethylamine on tyrosine uptake. At high concentrations, amphetamine and phenylethylamine lose their ability to stimulate dopamine synthesis and produce an antagonism of veratridine-induced synthesis stimulation.

Animals↗

PubMed1979

[Effect of beta-phenylethylamine on the dopaminergic system of rat brain].

Using a quantitative fluorescence-histochemical analysis the dynamics of changes of the dopamine level in dopaminergic neurons of the nigro-neostriatal and mesolimbic systems of the rat brain was studied during an hour after intraperitoneal injection of beta-phenylethylamine (100 mg/kg). The temporary increase in the dopamine level in the terminals coincided with a sharp decrease in the dopamine level in the neuron bodies, and conversely, the depletion of dopamine in the terminals after 30 min was accompanied by an increase in the dopamine level in the neuron bodies. The obtained results enable a suggestion that the increase in locomotor activity of animals after injection of beta-phenylethylamine described in the literature is due to the effect of phenylethylamine on catecholaminergic brain systems, the dopaminergic systems in particular.

Animals↗

PubMed1984

[beta-Phenylethylamine in the cisternal fluid in acute endogenous psychoses].

Beta-Phenylethylamine can be detected in the cisternal cerebrospinal fluid of healthy controls and acute endogenous psychoses. One group of the patients shows the same concentrations as the psychiatrically healthy controls. In the other groups beta-phenylethylamine was found to be elevated in some cases up to a very high level. The results suggest a link between a disturbance of the phenylethylamine pathway and certain endogenous psychoses.

Humans↗

PubMed1980

Comparative effects of substituted phenylethylamines on brain serotonergic mechanisms.

A series of substituted phenylethylamines were examined for their relative potencies to 1) release and inhibit accumulation of labeled serotonin in brain synaptosomes, 2) compete with serotonin receptor binding and 3) induce the "serotonin syndrome" in mice. In general, the relative potencies of the phenylethylamine derivatives to produce the serotonin syndrome did not correlates well with their effects on synaptosomal uptake or release of serotonin or serotonin receptor binding. However, para chloro substitution was more effective than meta or ortho chlorophenylethylamine and para methoxy substitution more effective than ortho methoxyphenylethylamine for [3H]serotonin uptake inhibition and release and induction of the serotonin syndrome. Lineweaver Burk kinetic analysis indicated that para chlorophenylethylamine was a competitive inhibitor of [3H]serotonin uptake in vitro with a Ki of 4.3 x 10(-7) M. Fluoxetine, a specific serotonin uptake inhibitor, blocked p-chlorophenylethylamine and p-methoxyphenylethylamine-induced [3H]serotonin release. The ability of phenylethylamine derivatives to release preferentially [3H]serotonin in vitro without damaging serotonergic neurons and to consistently and rapidly produce the serotonin syndrome in vivo should make these compounds useful pharmacological tools for investigating brain serotonin metabolism.

Animals↗

PubMed1994

Correlations of plasma and urinary phenylacetic acid and phenylethylamine concentrations with eating behavior and mood rating scores in brofaromine-treated women with bulimia nervosa.

Women with bulimia nervosa undergoing treatment with the reversible monoamine oxidase type A inhibitor, brofaromine, were rated for mood and eating behaviour and their plasma and urine were assessed for phenylacetic acid (unconjugated and total) and unconjugated phenylethylamine prior to and after four weeks of drug treatment. Changes in plasma unconjugated phenylacetic acid concentrations were significantly and negatively correlated with the corresponding changes in Hamilton Depression scores but not with eating behavior measures. There were no significant correlations between changes in phenylethylamine levels and changes in rating scores. Patients diagnosed as suffering concurrently from severe depression (Hamilton Depression score of 17 or higher) had lower plasma and urinary phenylacetic acid levels than did those whose depression was not severe (Hamilton score less than 17). Phenylethylamine concentrations were not different between the severely and mildly depressed subgroups. The results confirm earlier studies on the relationship between phenylacetic acid and depression while showing that a similar relationship does not pertain to phenylacetic acid and eating behavior in bulimia nervosa.

Adult↗

PubMed1988

Analysis of the pentafluorobenzoyl derivative of phenylethylamine utilizing negative ion chemical ionization and gas chromatography/mass spectrometry.

A negative ion chemical ionization (NICI) mass spectrometric procedure has been developed to measure phenylethylamine in human urine as the pentafluorobenzoyl derivative. The aromatic amine was isolated from alkaline urine by hexane and ethyl acetate extraction followed by a back-extraction into diluted acid. The acid extract was lyophilized and the residue derivatized with (2,3,4,5,6)-pentafluorobenzoyl chloride. Quantification was achieved by comparing the peak areas of the [M-HF]- ion to a ratio of internal and external standards. The phenylethylamine levels excreted by normal subjects and patients with phenylketonuria were found to be consistent with previous reports.

Benzoates↗

PubMed1986

Phenylethylamine-induced release of noradrenaline fails to stimulate alpha 1-adrenoceptors modulating [3H]-acetylcholine release in rat atria, but activates alpha 2-adrenoceptors modulating [3H]-serotonin release in the hippocampus.

The modulation of the depolarization induced release of [3H]-acetylcholine by agonists acting on alpha-adrenoceptors was studied in superfused rat atrial slices. In this model, noradrenaline and methoxamine, but not UK 14304 reduced the potassium evoked release of [3H]-acetylcholine. The inhibitory action of these drugs was antagonized by the alpha 1 selective adrenoceptor antagonist prazosin. Propranolol, idazoxan and sulpiride did not antagonize the inhibition by noradrenaline of the potassium-evoked release of [3H]-acetylcholine. Exposure to amphetamine, beta-phenylethylamine, m- or p-tyramine, increased in a concentration-dependent manner the spontaneous outflow of [3H]-noradrenaline from atrial slices. Yet, these concentrations of the indirectly acting sympathomimetic amines, tested in the presence of an inhibitor of monoamine oxidase (MAO), failed to modify the potassium evoked release of [3H]-acetylcholine. Desipramine 3 mumol/l or cocaine 10 mumol/l did not affect the release of [3H]-acetylcholine evoked by potassium stimulation. Under similar experimental conditions, beta-phenylethylamine facilitated the spontaneous outflow of [3H]-noradrenaline, and inhibited the electrically-evoked release of [3H]-serotonin from the hippocampus by activation of alpha 2-adrenoceptors. It is concluded that the release of acetylcholine from atrial cholinergic neurons can be modulated through inhibitory alpha 1-adrenoceptors, which are not activated when the release of noradrenaline is induced by indirectly acting sympathomimetic amines. In addition, amphetamine or structurally related amines do not activate directly recognition sites in the cholinergic postganglionic parasympathetic neuron to modify the release of [3H]-acetylcholine.

Acetylcholine↗

PubMed1993

Determination of regional distributions of phenylethylamine and meta- and para-tyramine in rat brain regions and presence in human and dog plasma by an ultra-sensitive negative chemical ion gas chromatography-mass spectrometric (NCI-GC-MS) method.

Using a new ultrasensitive method the trace biogenic amines, phenylethylamine, meta-tyramine and para-tyramine have been quantitated in brain regions obtained from a single rat. Phenylethylamine concentrations in ng/g wet tissue (mean +/- std. error) were as follows: caudate 2.71 +/- 0.73, hypothalamus 0.45 +/- 0.15, cerebellum 0.09 +/- 0.02, olfactory bulb 0.35 +/- 0.11, stem 0.13 +/- 0.03, hippocampus 0.20 +/- 0.11, cortex 0.69 +/- 0.13 and the rest (remainder of the brain) 2.81 +/- 0.41. Mean whole brain was 1.23 +/- 0.19 ng/g, in agreement with previous measurements. meta-Tyramine concentrations (ng/g) were: caudate 2.69 +/- 0.19, hypothalamus 0.32 +/- 0.16, cerebellum 0.07 +/- 0.04, olfactory bulb 0.09 +/- 0.04, stem 0.04 +/- 0.01, hippocampus 0.07 +/- 0.02, cortex 0.18 +/- 0.15 and the rest 0.15 +/- 0.06, with a mean whole brain value of 0.26 +/- 0.05 ng/g and para-tyramine concentrations were: caudate 8.99 +/- 1.60, hypothalamus 0.93 +/- 0.13, cerebellum 0.78 +/- 0.27, olfactory bulb 0.70 +/- 0.13, stem 0.90 +/- 0.36, hippocampus 0.40 +/- 0.06, cortex 1.78 +/- 0.28 and the rest 2.38 +/- 0.12 and mean whole brain was 1.90 +/- 0.25 ng/g. In human plasma the concentrations of the three amines were found to be 31.3 +/- 3.4 pg/ml, 5.3 +/- 1.6 pg/ml and 66.0 +/- 9.9 pg/ml respectively and in dog blood 95.3 +/- 4.6 pg/ml, 24.0 +/- 7.6 pg/ml and 486 +/- 43 pg/ml respectively. When monoamine oxidase inhibitors were added to the blood immediately after collection there were no significant increases in the amine levels indicating that MAO-B is not present in plasma in significant quantities.

Animals↗

PubMed1993

Investigations into the biochemical basis of neuromodulation by 2-phenylethylamine: effect on microtubule protein.

In order to understand the role of 2-phenylethylamine (PE) on neuronal responses, membrane changes have been studied using ESR probes. We report that the anticipated change in lipid membrane fluidity generally implicated in signal transduction has not been observed when PE is added to synaptosomes. As cytoskeletal architecture of presynaptic terminals appears to be involved in synaptic transmission, we non-specifically labeled synaptosomal membrane proteins with the sulfhydryl spin probe N-(2,2,6,6-tetramethyl-piperidine-1-oxyl-4-yl) maleimide (4-MAL-TEMPO). The addition of 2-phenylethylamine was found to induce conformational changes, in decreasing the ratio of weakly to strongly immobilized spin label (W/S) to 65% of the control. Of the membrane proteins labeled, 70-90% of the 4-MAL-TEMPO is covalently incorporated into cytoskeletal proteins. In isolated synaptosomes, incorporated with spin-labeled tubulin, the addition of PE reduced the W/S ratio to 51.6% of that obtained for polymerized microtubules. In vitro, PE reduced tau R of polymerized microtubules by 37%. We propose that the PE interaction with tubulin changes microtubule dynamics which may lead to its neuromodulatory action. The state of microtubular assembly can modulate the responsiveness of second messengers in the cell to the effect of stimulatory agents. The nature and physiological significance of PE interaction with tubulin is currently under investigation.

Animals↗

PubMed1993

The potentiation of cortical neuron responses to noradrenaline by 2-phenylethylamine is independent of endogenous noradrenaline.

2-Phenylethylamine (PE) is an endogenous brain amine which produces sympathomimetic responses and potentiates cortical neuron responses to noradrenaline (NA). In order to examine further the mechanism of action of PE, extracellular recordings were made of the activity of single neurones in the cerebral cortex in urethane-anesthetized rats. Sympathomimetic responses to PE were blocked by pretreatment with reserpine, reserpine plus alpha-methyl-p-tyrosine and desipramine. It is concluded that the sympathomimetic responses to PE are indirect. 2-Phenylethylamine potentiated cortical neuron responses to electrical stimulation of the locus coeruleus in a dose-dependent manner. This was seen when PE was given systemically (with as little as 1 microgram/kg) and iontophoretically. The effects of PE were not reproduced by its metabolite phenylacetic acid or its putative metabolite phenylethanolamine. Iontophoretic applications of PE (0-6 nA, 2-5 minutes) potentiated cortical neuron responses to iontophoretically applied NA, without affecting the spontaneous firing rate, or the responses to iontophoretically applied GABA or acetylcholine. This effect of PE was not blocked by pretreatment with alpha-methyl-p-tyrosine or desipramine, and was potentiated by pretreatment with reserpine and reserpine plus alpha-methyl-p-tyrosine. It is probable that the ability of PE to modulate neuronal responses to NA does not involve the presynaptic NA terminal or endogenous NA and it is likely that PE acts directly to increase the efficacy of NA. These findings are consistent with the hypothesis that the physiological role of PE is to modulate catecholaminergic transmission within the central nervous system.

Animals↗

PubMed1992

[Occurrence of beta-phenylethylamine and its derivatives in cocoa and cocoa products].

2-Phenylethylamine was extracted from cocoa nibs and chocolates and analysed by coupled gas chromatography-mass spectroscopy. The amine concentration increases in fermentation of cocoa and decreased during roasting and alkalization. Its concentration in chocolates is dependent on non-fat cocoa contents. Previously unreported aldimines were found in cocoa powders, which arise from the condensation of phenylethylamine and aldehydes. The main component of these products is N-phenylmethyl-N-phenylmethylene amine (CAS 3240-95-7).

Cacao↗

PubMed1986

Determination of beta-phenylethylamine concentrations in human plasma, platelets, and urine and in animal tissues by high-performance liquid chromatography with fluorometric detection.

A highly sensitive method for the determination of beta-phenylethylamine in human plasma, platelets, and urine and in mouse tissue is described. The method is based on a two-step isolation using cation-exchange columns followed by reverse phase high-performance liquid chromatography with fluorometric detection. The recovery of the amine through the whole procedure was almost complete, ranging from 99 to 101%. The calibration graph appeared linear over the range of 50 to 5000 pg/injection. Urinary excretion of beta-phenylethylamine in humans ranged from 0.93 to 51.20 ng/mg creatinine. The amine was also detectable in plasma and platelets. Of the various mouse tissues examined, the highest concentrations were found in the small intestine, followed by the blood and liver. Concentrations of about 5 ng/g wet wt were detected in brain tissue, which increased remarkably after inhibition of monoamine oxidase by pargyline.

Animals↗

PubMed1985

Formation of beta-phenylethylamine from the antidepressant, beta-phenylethylhydrazine.

To determine whether the monoamine oxidase inhibitor phenelzine was metabolized in vivo to produce beta-phenylethylamine (PE) and p-hydroxy-beta-phenylethylamine [p-tyramine (pTA)], a deuterated analogue, alpha, alpha,, beta, beta-2H-phenelzine (d4-phenelzine) was synthesized and injected i.p. into rats. In the first experiment, rat striata from d4-phenelzine-treated rats were analyzed for the presence of d4-PE and d4-pTA at a time at which phenelzine was known to cause particularly large increases in striatal pTA. While d4-PE was found to be present in these rat striata at a concentration equivalent to the endogenous PE, no d4-pTA was present. The amounts of d4-PE produced at various times after the i.p. injection of 50 mg/kg d4-phenelzine were measured; at 1 hr post-injection, 371 +/- 60, 1295 +/- 682 and 1242 +/- 394 ng/g (mean +/- S.E.M.) d4-PE were present in whole brain, liver and kidney. Rat urine collected for a 24-hr period after this treatment contained (mean +/- S.E.M.) 88.5 +/- 14.0 micrograms d4-PE. These results clearly indicate that the antidepressant phenelzine was metabolized in vivo to produce the trace amine PE.

Animals↗

PubMed1976

Pathways linking L-phenylalanine and 2-phenylethylamine with p-tyramine in rabbit brain.

Concentrations of labeled p-tyramine and 2-phenylethylamine were measured in rabbit brain 10 min after the intraventricular administration of either radioactive amine. In both cases the recoveries of the newly synthesized amine and of the unchanged precursor were significantly increased in animals pretreated with the monoamine oxidase inhibitor pargyline. Significant amounts of both amines were present in rabbit brain 10 min after the intraventricular injection of labeled L-phenylalanine. Pretreatment with pargyline increased their recoveries, whereas alpha-methyldopa (an L-aromatic amino acid decarboxylase enzyme inhibitor, L-AAADI) decreased them considerably, and no significant alteration was found in L-alpha-methyldopa hydrazine (a peripheral L-AAADI) pretreated animals. These results provide evidence for a new biochemical pathway in brain for p-tyramine biosynthesis, with L-phenylalanine (bypassing the formation of L-tyrosine) or 2-phenylethylamine as precursors. The significance and implications of these metabolic routes are discussed, especially considering that p-tyramine itself can be converted to catecholamines.

Animals↗

PubMed1976

A method for the estimation of 2-phenylethylamine in human urine by gas chromatography.

A gas chromatographic procedure with flame ionisation detection has been developed to measure 2-phenylethylamine in human urine as the trifluoroacetyl derivative. The amine is purified by an ether extraction procedure and derivatised with trifluoroacetic anhydride. Quantification is obtained by comparing the peak height with that for an internal standard added to the urine before extraction. The normal 24-h excretion value for 2-phenylethylamine in human urine is found to be 6.8 +/- 2.9 mug (mean +/- S.D.).

Adolescent↗

PubMed1975

The monoamine oxidase B inhibitor deprenyl potentiates phenylethylamine behaviour in rats without inhibition of catecholamine metabolite formation.

The drug l-deprenyl has been reported to have antidepressant properties, and in the present study three possible mechanisms of action were investigated in animal experiments. l-Deprenyl, which is a type B monoamine oxidase (MAO) inhibitor, was compared to clorgyline, an MAO A inhibitor with regard to its inhibitory effect on the formation of three major catecholamine metabolites, homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylglycol (MOPEG) in the rat brain in vivo. Apart from a difference in dose levels the two drugs showed no difference in the dose--response pattern of all three metabolites. Clorgyline inhibited the formation of HVA, DOPAC and MOPEG with an ED50 of about 0.2 mg/kg s.c. and l-deprenyldopamine and noradrenaline are formed by the same type of monoamine oxidase(s), probably type A, in the rat brain in vivo. Antidepressant properties of l-deprenyl therefore seem to be independent of catecholamine deamination. l-Deprenyl but not clorgyline (2 or 8 mg/kg s.c.) potentiated the stereotyped sniffing behaviour induced by beta-phenylethylamine, a specific substrate for type B monoamine oxidase. This result is discussed in relation to a new hypothesis of phenylethylamine and dopamine involvement in depression. l-Deprenyl was 10,000 times less potent than DMI as inhibitor of noradrenaline uptake in crude synaptosomes from the occipital cortex of rat brain. Inhibition of noradrenaline uptake was therefore excluded as a possible mechanism for the antidepressant action of l-deprenyl.

Animals↗

PubMed1985

Caffeine-phenylethylamine combinations mimic the amphetamine discriminative cue.

Although caffeine-phenylethylamine combinations are widely available as over-the-counter medications or as "legal" stimulants, little information is available concerning their behavioral pharmacology or abuse potential. In the present study, rats were trained in a food-reward, two-lever operant drug discrimination paradigm to differentially respond after saline or 0.5 mg/kg amphetamine injections. Tests for generalization to the amphetamine cue indicated only modest amphetamine-lever responding at various doses of caffeine alone or at various doses of ephedrine/phenylpropanolamine (PPA) combinations, but complete generalization to the training cue was found with higher doses of the triple combination (caffeine, ephedrine, and PPA) or with caffeine-ephedrine or caffeine-PPA combinations. All drugs produced response rate decreases at higher doses. These data clearly indicate that certain "legal" stimulants mimic the amphetamine cue and suggest that caffeine may interact additively with phenylethylamines to produce the cue.

Amphetamine↗