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PubMed1983

The biosynthesis of p-tyramine, m-tyramine, and beta-phenylethylamine by rat striatal slices.

Slices of striatal tissue obtained from saline-injected rats were incubated with 3H-phenylalanine in the presence of pargyline. This resulted in the formation of 3H-m-tyramine, 3H-p-tyramine, and 3H-phenylethylamine. Pretreatment of the rats with alpha-methyl-p-tyrosine reduced the formation of 3H-m-tyramine and 3H-p-tyramine, but enhanced the formation of 3H-phenylethylamine. After incubation of striatal tissue obtained from saline-injected rats with 3H-ptyrosine, only 3H-p-tyramine was produced. In this case, alpha-methyl-p-tyrosine pretreatment enhanced 3H-p-tyramine formation. Striatal slices incubated with 3H-m-tyramine or 3H-p-tyramine did not yield any significant quantity of 3H-phenylethylamine; nor was 14C-phenylethylamine converted to 14C-m-tyramine or 14C-p-tyramine. Pretreatment of the rats with the monoamine oxidase inhibitor pargyline did not appreciably affect these findings. After incubation with 3H-dopamine very small quantities of 3H-m-tyramine and 3H-p-tyramine were formed, the ratio between them being 7:1. It is concluded that the major biosynthetic route for m-tyramine formation in the rat striatum is by hydroxylation of phenylalanine, probably by tyrosine hydroxylase to m-tyrosine, followed by decarboxylation, probably by L-aromatic amino acid decarboxylase, to m-tyramine. para-Tyramine is formed by decarboxylation of p-tyrosine, and phenylethylamine similarly by decarboxylation of phenylalanine.

Animals↗

PubMed1987

In vivo release of endogenous dopamine, 5-hydroxytryptamine and some of their metabolites from rat caudate nucleus by phenylethylamine.

The in vivo release of endogenous 3,4-dihydroxyphenylethylamine (DA) and its metabolites, 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA) and 3-methoxytyramine (3-MT), and of 5-hydroxytryptamine (5-HT) and its metabolite, 5-hydroxyindoleacetic acid (5-HIAA), has been measured in the caudate nucleus of the anesthetized rat. A push-pull cannula was implanted into the brain, and the tissue perfused with artificial CSF or artificial CSF containing 5 X 10(-4) M phenylethylamine. The perfusate was collected and analyzed for DA, 5-HT and their metabolites by high performance liquid chromatography with electrochemical detection (HPLC-ECD). DA was released by phenylethylamine at rates significantly greater than its basal rate. 3-MT and 5-HT were undetectable in perfusates collected under basal conditions, but could be detected readily during phenylethylamine stimulation. DOPAC, HVA and 5-HIAA concentrations were not significantly affected by phenylethylamine. The results suggest (1) that phenylethylamine may exert its behavioural effects through increased release of both DA and 5-HT, and (2) that in vivo measurements of the acid metabolites alone may not be indicative of the release of the amines.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1978

The uri nary excretion of 2-phenylethylamine in phenylketonuria.

The urinary concentrations of free and conjugated 2-phenylethylamine were determined in phenylketonuric patients and normal subjects by solvent extraction and gas chromatography. Free 2-phenylethylamine excretion was found to be significantly elevated above normal in phenylketonuric adults and children receiving a normal or a slightly restricted intake of phenylalanine. Urinary 2-phenylethylamine was also significantly increased in phenylketonuric children receiving low phenylalaine dietary therapy. Conjugated 2-phenylethylamine excretion was found not to be increased above normal. In the light of these results, a relationship between blood phenylalanine concentration and 2-phenylethylamine excretion is proposed, and the possible role of this amine in phenylketonuria is discussed.

Adult↗

PubMed1988

Chronic cocaine effects on peripheral biogenic amines: a long-term reduction in peripheral dopamine and phenylethylamine production.

The short- (during 12 h after last treatment) and long- (6 weeks after last treatment) term effects of repeated administration of cocaine on the total output of norepinephrine (NE) and its metabolites (sum NE), dopamine (DA) and its metabolites (sum DA) as well as the excretion of 5-hydroxyindoleacetic acid (5-HIAA) and phenylethylamine were evaluated in rats. The concentration of NE, DA and 3,4-dihydroxyphenylacetic acid (DOPAC) in the celiac ganglion after 1, 2 and 3 weeks of repeated cocaine administration were also measured. Sum NE remained unchanged during the cocaine treatment but NE and normetanephrine excretions were significantly decreased and increased respectively. 5-HIAA excretion was significantly reduced only after 3 weeks cocaine treatment. In the celiac ganglion NE and DOPAC contents showed tendencies towards being increased and decreased respectively. DA content was not changed. The excretions of DA, DOPAC, homovanillic acid (HVA) and phenylethylamine were significantly reduced during chronic exposure to cocaine. The above short-term changes in DA and phenylethylamine persisted for periods as long as 6 weeks after 1 week repeated exposure to cocaine. It is concluded that chronic exposure to cocaine can produce preferential long term deficiencies in the production of DA and phenylethylamine in the periphery. Peripheral noradrenergic and serotonergic neuronal systems are apparently minimally affected. The close association between DA or sum DA and phenylethylamine excretion suggest these 2 amines may coexist in the same neuron.

3,4-Dihydroxyphenylacetic Acid↗

PubMedDate not supplied

Characteristic of analgesia induced by noncatecholic phenylethylamines in mice.

Using hot plate method, analgesia induced by noncatecholic phenylethylamines, phenethylamine, phenylethanolamine and amphetamine, was inhibited by naloxone, reserpine, apomorphine and p-chlorophenylalanine, while potentiated by haloperidol. These results suggest that phenylethylamines induced analgesia involves central dopaminergic and serotonergic neurons and endogenous opioid peptides. The blockade of dopaminergic neurons enhanced and the inhibition of serotonergic neuron activity or the stimulation of dopaminergic neurons attenuated the phenylethylamines induced analgesia. Using rat hind paw pressing or tail flick test, analgesia induced by electroacupuncture in which Hoku points were electrically stimulated through stainless steel needles was enhanced by phenylethylamines, haloperidol while attenuated by naloxone, reserpine, apomorphine and p-chlorophenylalanine. Thus the analgegic characteristic of phenylethylamines closely resembles that of electroacupuncture.

2-Hydroxyphenethylamine↗

PubMed1984

Potentiation of total horizontal activity and ambulation in rats treated with combinations of beta-phenylethylamine and naloxone.

The effects of beta-phenylethylamine (PEA) (6.25-50 mg kg-1) and of naloxone (1-10 mg kg-1), administered alone and in combination, were studied in the rat. Adult, male rats were individually tested in a novel enclosure over a 30 min period, after administration of drugs. Measures of total horizontal activity, ambulation and rearing activity were counted automatically on the basis of interruptions of photobeams. In addition, observational data were collected, using behavioural categories which have previously been used to characterize the behavioural stereotypy syndrome induced by phenylethylamine in large doses. The results showed that certain combinations of phenylethylamine and naloxone produced striking increases in total horizontal activity and ambulation scores, but not in vertical activity scores. Furthermore, naloxone antagonized hyperreactivity and splayed-hindlimb components of the stereotypy syndrome induced by phenylethylamine, but not the head-weaving component. The behavioural specificity of the potentiation of total horizontal activity and ambulation by phenylethylamine in combination with naloxone is emphasized, and the enhancement of activity is contrasted with previous reports of the effects of naloxone administered in conjunction with d-amphetamine.

Amphetamine↗

PubMed1984

beta-Phenylethylamine and reinforcement.

beta-Phenylethylamine is an endogenous brain amine which has been characterised as an endogenous amphetamine. The rewarding properties of the structurally similar drug amphetamine in humans and other species indicate a possible role for endogenous beta-phenylethylamine in neural processes underlying reward or reinforcement. Evidence for reinforcing properties of beta-phenylethylamine in the drug self-administration and place preference paradigms is briefly reviewed. The possibility that endogenous beta-phenylethylamine may be involved in reinforcement processes is also considered in relation to studies of intracranial self-stimulation. The contrasting aversive stimulus properties of beta-phenylethylamine and of amphetamine are described.

Animals↗

PubMed2006

Contribution of aldehyde oxidizing enzymes on the metabolism of 3,4-dimethoxy-2-phenylethylamine to 3,4-dimethoxyphenylacetic acid by guinea pig liver slices.

BACKGROUND/AIMS: 3,4-Dimethoxy-2-phenylethylamine is catalyzed to its aldehyde derivative by monoamine oxidase B, but the subsequent oxidation into the corresponding acid has not yet been studied. Oxidation of aromatic aldehydes is catalyzed mainly by aldehyde dehydrogenase and aldehyde oxidase. METHODS: The present study examines the metabolism of 3,4-dimethoxy-2-phenylethylamine in vitro and in freshly prepared and cryopreserved guinea pig liver slices and the relative contribution of different aldehyde-oxidizing enzymes was estimated by pharmacological means. RESULTS: 3,4-Dimethoxy-2- phenylethylamine was converted into the corresponding aldehyde when incubated with monoamine oxidase and further oxidized into the acid when incubated with both, monoamine oxidase and aldehyde oxidase. In freshly prepared and cryopreserved liver slices, 3,4-dimethoxyphenylacetic acid was the main metabolite of 3,4-dimethoxy-2- phenylethylamine. 3,4-Dimethoxyphenylacetic acid formation was inhibited by 85% from disulfiram (aldehyde dehydrogenase inhibitor) and by 75-80% from isovanillin (aldehyde oxidase inhibitor), whereas allopurinol (xanthine oxidase inhibitor) inhibited acid formation by only 25-30%. CONCLUSIONS: 3,4- Dimethoxy-2-phenylethylamine is oxidized mainly to its acid, via 3,4-dimethoxyphenylacetaldehyde, by aldehyde dehydrogenase and aldehyde oxidase with a lower contribution from xanthine oxidase.

Aldehyde Oxidase↗

PubMed1990

Phenylethylamine metabolism in Tourette's syndrome.

Beta-phenylethylamine, phenylalanine, and phenylacetic acid were examined in 24-hour urine samples and/or plasma samples obtained from 28 medication-free patients with Tourette's syndrome and 20 control subjects matched for age and education. Statistical analyses revealed that Tourette patients had lower plasma phenylalanine and urinary free beta-phenylethylamine compared with the controls, but did not differ on urinary total levels of phenylacetic acid. Fifty percent of the Tourette patients had a urinary beta-phenylethylamine level that was lower than the lowest control subject. In addition, urinary beta-phenylethylamine levels were inversely related to several scores from the Tourette Syndrome Global Scale. These data suggest that abnormalities in synthesis or metabolism of beta-phenylethylamine may be involved in the etiology of some patients with Tourette's syndrome.

Child↗

PubMed1976

Dose-response effects of beta-phenylethylamine on stereotyped behavior in pargyline-pretreated rats.

We studied the dose-response and the time-course effect of beta-phenylethylamine (4.0-64.0 mg/kg, ip) on stereotyped behavior and motor activity in male Sprague-Dawley rats pretreated 2 hr eariler with pargyline (0.25-8.0 mg/kg, iv). Stereotyped behavior, defined as repetitive, nongoal-directed head movements and sniffing, and changes in motor activity were observed immediately after injection of beta-phenylethylamine for a 1 hr period. With increasing doses of pargyline pretreatment, beta-phenylethylamine produced, in a dose-response relationship, progressively more stereotyped behavior accompanied by increased motor activity. Without pargyline pretreatment, only 64.0 mg/kg beta-phenylethylamine induced behavioral changes. Stereotyped behavior and increased motor activity had an onset at 4-6 min after the injection of beta-phenylethylamine, peak at 10-30 min, and gradual decline in the next 10-20 min. These results are discussed in terms of a possible relationship with the degree of inhibition of Type a and Type B monoamine oxidase acused by the different doses of pargyline.

Animals↗

PubMed1991

Variation in the interaction of some phenylethylamine and imidazoline derivatives with alpha-1 adrenoceptors in rabbit arteries: further evidence for the variable receptor affinity hypothesis.

This study was undertaken to determine whether the variation in the affinity of the alpha-1 adrenoceptors previously found for norepinephrine and phenylephrine in different arteries is also seen with other alpha-1 adrenoceptor agonists, and if so, if one part of the structure is particularly responsible for the variation. The potency and dissociation constants of eight agonists, both phenylethylamines and imidazolines, were determined in five rabbit arteries. In each artery the rank order of phenylethylamine agonist potency was epinephrine greater than norepinephrine greater than phenylephrine greater than deoxyepinephrine greater than methoxamine greater than dopamine. The same rank order of dissociation constants was found. For the imidazolines, the potency order was oxymetazoline greater than clonidine. For each agonist, there was a linear correlation between artery sensitivity and receptor affinity. None of the regression line slopes differed from each other. For each artery there was a linear correlation between phenylethylamine sensitivity and affinity. With the exception of the ovarian, which was lower, slopes of the regression lines in each group do not differ from each other. There were differences in the spread of the dissociation constants of the phenylethylamine derivatives among the arteries. The range of affinities was most marked with norepinephrine (greater than 40-fold) and least with epinephrine (approximately 4-fold). They suggest that agonist affinity governs the biological activity of at least the phenylethylamines on rabbit arteries mediated by the alpha-1 adrenoceptor. Variation in agonist affinity can explain the extent of the biological response. Differences in range of amine affinities in different arteries suggest that the agonist recognition site, although similar in the different arteries, is not identical and may be related particularly to some variation of the amine attachment site of the molecule. The results provide further support for the variable receptor affinity hypothesis.

Animals↗

PubMed1983

Determination of beta-phenylethylamine as its isothiocyanate derivative in biological samples by gas chromatography mass spectrometry.

A detailed procedure of a gas chromatographic mass spectrometric assay for beta-phenylethylamine in biological samples, after its reaction with carbon disulphide to form the isothiocyanate derivative, is presented. Our method has advantages over the previous methods with the pentafluoropropionic derivative of beta-phenylethylamine in that the isothiocyanate derivative of beta-phenylethylamine is much more stable than the pentafluoropropionic derivative and that the background in selected ion monitoring is very low. Using the present method, the levels of beta-phenylethylamine in human urine, untreated and pargyline-treated rat brain were found to be 15.3 micrograms 24 h-1, 1.4 and 160 ng g-1 wet weight, respectively.

Animals↗

PubMed1991

Quantification of plasma phenylethylamine by combined gas chromatography/electron capture negative ion mass spectrometry of the N-acetyl-N-pentafluorobenzoyl derivative.

An ultrasensitive method capable of detection and quantification of beta-phenylethylamine in 1 ml of human plasma has been developed using gas chromatography/electron capture negative ion mass spectrometry. Phenylethylamine and tetra-deutero phenylethylamine internal standard in plasma were acetylated, extracted into organic solvent and then further acylated with pentafluorobenzoyl chloride. The N-acetyl-N-pentafluorobenzoyl-phenylethylamines were detected by high-resolution single ion monitoring of the molecular ions. Normal plasma levels were found to be 41.5 +/- 10.7 pg ml-1, in accordance with results of a previous high-performance liquid chromatographic method.

Chromatography, Gas↗

PubMed2007

Enhanced efficiency due to the use of achiral additives in the optical resolution of 1-phenylethylamine by its glutaric acid derivative.

Racemic 1-phenylethylamine was optically resolved by its own derivative formed with glutaric acid namely (+)-(R)-N-(1-phenylethyl)glutaramic acid. The amide acid resolving agent was synthesized from (+)-(R)-1-phenylethylamine by N-derivatization. The glutaric acid derivative was the next in a homologous series of dicarboxilic acid derivatized resolving agents of racemic 1-phenylethylamine. Resolution results obtained with the oxalic, malonic, and succinic acid derivatives were previously discussed(1). Each of the above derivative resolving agents could be successfully applied as resolving agents of 1-phenylethylamine. The efficiency of the present optical resolution using (+)-(R)-N-(1-phenylethyl)glutaramic acid resolving agent was remarkably inferior to the results obtained by its shorter chained homologues(1). Use of achiral additives, like urea, thiourea, N-methylurea, and N,N'-dimethylurea caused large increase in the efficiency of the resolution by (+)-(R)-N-(1-phenylethyl)glutaramic acid resolving agent. Precipitated salts obtained in the resolutions performed in the presence of the additives were investigated by thermoanalysis, X-ray powder diffraction, and optical microscopy. Based on the analytical data, the improvement of the resolution results was attributed to the influence of the additives on the crystal nucleation processes of the diasteromeric salts.

Journal Article↗

PubMed1977

Desynchronization of electrical activity in rats induced by deprenyl--an inhibitor of monoamine oxidase B--and relationship with selective increase of dopamine and beta-phenylethylamine.

Electrophysiological and biochemical effects of deprenyl and beta-phenylethylamine were studied in rats. d,1-Deprenyl, 1-deprenyl (4-6 mg/kg) and beta-phenylethylamine (75 mg/kg) induced a desynchronization of ECOG after i.p. administration of drugs. The effects lasted several hours. The biochemical analysis indicate that d,1-deprenyl (4 mg/kg) nearly doubled the concentration of brain dopamine (DA) while the concentration of noradrenaline was not altered. The maximal increase was reached at 60 min and the enhanced concentration of DA stayed at this level up till 180 min after administration of drug. Treatment of rats with alpha-methyl-p-tyrosine (200 mg/kg) did not antagonize a deprenyl induced desynchronization of ECOG. However, even low dose of haloperidol (0.1 mg/kg) abolished the arousal effect of d,1-deprenyl and beta-phenylethylamine. It is suggested that desynchronization of EEG induced by deprenyl is more likely due to increased endogenous beta-phenylethylamine than to increased concentration of endogenous DA in the brain.

Acoustic Stimulation↗

PubMedDate not supplied

Metabolism of 2-phenylethylamine and phenylacetaldehyde by precision-cut guinea pig fresh liver slices.

2-Phenylethylamine is an endogenous constituent of human brain and is implicated in cerebral transmission. It is also found in certain foodstuffs and may cause toxic side-effects in susceptible individuals. Metabolism of 2-phenylethylamine to phenylacetaldehyde is catalyzed by monoamine oxidase and the oxidation of the reactive aldehyde to its acid derivative is catalyzed mainly by aldehyde dehydrogenase and perhaps aldehyde oxidase, with xanthine oxidase having minimal transformation. The present investigation examines the metabolism of 2-phenylethylamine to phenylacetaldehyde in liver slices and compares the relative contribution of aldehyde oxidase, xanthine oxidase and aldehyde dehydrogenase activity in the oxidation of phenylacetaldehyde with precision-cut fresh liver slices in the presence/absence of specific inhibitors of each enzyme. In liver slices, phenylacetaldehyde was rapidly converted to phenylacetic acid. Phenylacetic acid was the main metabolite of 2-phenylethylamine, via the intermediate phenylacetaldehyde. Phenylacetic acid formation was completely inhibited by disulfiram (specific inhibitor of aldehyde dehydrogenase), whereas isovanillin (specific inhibitor of aldehyde oxidase) inhibited acid formation to a lesser extent and allopurinol (specific inhibitor of xanthine oxidase) had little or no effect. Therefore, in liver slices, phenylacetaldehyde is rapidly oxidized by aldehyde dehydrogenase and aldehyde oxidase with little or no contribution from xanthine oxidase.

Acetaldehyde↗

PubMed1995

beta-Phenylethylamine regulation of dopaminergic nigrostriatal cell activity.

In the present paper, the action of beta-phenylethylamine on electrophysiological activity of dopaminergic nigrostriatal neurons is described. 10 s after its i.v. injection and during 2-4 min, beta-phenylethylamine decreased the firing rate, the number of spikes within and out of burst and the number of bursts per second of these neurons. This was a dose-related action with statistical differences starting from 1.4 mg/kg for total and out of burst firing rate and from 2.4 mg/kg for within burst firing rate and for the number of bursts per second. The standard deviation and the variation coefficient of inter-spike intervals increased in a dose-related way. The marked effect found after low-dose administration suggests that under physiological conditions endogenous beta-phenylethylamine levels regulate the nigrostriatal dopaminergic cell activity. After peripheral low dose administration, beta-phenylethylamine behaves as a dopaminergic agonist with a very fast and brief action.

Action Potentials↗

PubMed1985

[3H] beta-phenylethylamine but not [3H](+)-amphetamine is released by electrical stimulation from perfused rat striatal slices.

Perfused rat striatal slices were prelabelled with either [3H](+)-amphetamine or [3H] beta-phenylethylamine. Electrical stimulation released a significant amount of radioactivity only from the slices prelabelled with [3H] beta-phenylethylamine. The electrically evoked release of radioactivity from slices labelled with [3H] beta-phenylethylamine was entirely calcium-dependent and was abolished after pretreatment with reserpine (5 mg/kg s.c., 24 h). In addition, S-sulpiride (1 microM), which facilitates the electrically evoked release of radioactivity from slices labelled with [3H]DA by blocking dopamine autoreceptors, also induced an increase of the radioactivity released by electrical stimulation from slices labelled with [3H] beta-phenylethylamine. Our results indicate that, in spite of the structural similarities between AMPH and PEA, only the latter which is the naturally occurring analog of AMPH can be released by electrical stimulation in a calcium-dependent manner.

Amphetamine↗