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PubMed1980

Effect of some beta-carbolines on phenylethylamine and apomorphine stereotypies in rats.

Tetrahydro-beta-carbolines (THBC:s) have recently been shown to occur in the human body and their role in mental diseases has been discussed. The effect of THBC:s and some other beta-carbolines (25 mg/kg IP) were studied on the stereotypies caused by apomorphine (APO, 2 mg/kg IP) and phenylethylamine (PEA, 50 mg/kg IP) in rats. These effects of dopaminergic drugs like apomorphine as well as of phenylethylamine have sometimes been used as animal models of paranoid schizophrenia. Dose effect relationships were studied from ther most potent substances. All beta-carbolines studied significantly inhibited APO stereotypy. 6-Methoxyharmalan was most effective followed by beta-carboline (BC), tetrahydro-beta-carboline (THBC), 1-methyl-THBC, 6-methoxy-THBC and 6-hydroxy-THBC. 6-Methoxyharmalan, 6-hydroxy-THBC and BC inhibited also PEA stereotypy. Other substances studied were ineffective. beta-Carbolines did not inhibit PEA and APO stereotypies in the same way. Thus the mode of PEA and APO stereotypies seems to differ, and beta-carbolines seem influence these stereotypies by more than one mechanism. If dopamine hypothesis is valid, the beta-carbolines formed in human body may protect rather than worsen in paranoid psychoses.

Aggression↗

PubMed1983

Deuterium substitution enhances the effects of beta-phenylethylamine on spontaneous motor activity in the rat.

The effects of beta-phenylethylamine (PEA) and alpha, alpha, beta, beta-tetradeutero-beta-phenylethylamine (deuterated PEA) on spontaneous motor activity and conditioned taste aversion learning in the rat were examined. The intensity and duration of certain behavioural components elicited by PEA, namely, sniffing, headweaving, splayed hindlimbs and hyperreactivity, were significantly increased by deuterium substitution. In contrast, deuteration had no effect on the ability of PEA to elicit a conditioned taste aversion. The potentiation of the amine's effects on activity seemed to be directly related to the longer persistence of PEA in the brain due to the kinetic isotope effect since it appears that tetra-deuterated PEA is a poorer substrate for monoamine oxidase than the protonated amine.

Animals↗

PubMed1984

Phenylethylamine, norepinephrine and mounting behavior in the male rat.

Phenylethylamine, which induces mounting behavior in naive adult male rats when administered chronically, was shown to selectively raise brain norepinephrine levels in the medial preoptic nucleus, a region known to be implicated in the regulation of sexual behaviors. It is suggested that the catecholamine alteration is a secondary response to the primary influence of phenylethylamine on the preoptic nucleus.

Animals↗

PubMed1983

The effects of beta-phenylethylamine and phenylethanolamine on water intake in rats: a temporal analysis.

Male Wistar rats were adapted to a restricted access schedule of water intake. For each animal overall water intake (ml) and number of licks per minute were measured over the period of access to water. The effects of various doses of beta-phenylethylamine and of phenylethanolamine were assessed in separate groups of animals. In terms of effects on overall consumption the two amines were equipotent in suppressing water intake. The local analysis revealed, however, that beta-phenylethylamine was more potent, but had a much shorter duration of action than phenylethanolamine.

2-Hydroxyphenethylamine↗

PubMed1983

Studies in the mechanism of phenylethylamine uptake by rabbit erythrocytes.

The mechanism of phenylethylamine (PEA) uptake by in vitro rabbit erythrocyte preparations involve both a larger component of passive diffusion and an Na+-dependent facilitated transport system. This is reflected by the fast rate and lack of saturation of PEA erythrocyte uptake, and by the decrease in PEA tissue/medium ratio when the amine was incubated in an Na+-free medium or in the presence of ouabain. Results obtained after the addition of iodoacetamide or by the use of glucose-free medium suggest the Na+-K+ gradient as the driving force responsible for operation of the carrier mechanism. Preliminary results indicate that amphetamine PEA share a similar mechanism for their uptake by rabbit erythrocytes. At the levels normally present in rabbit blood (c. 1 X 10(-8)M), about one-third of the PEA is found in the serum and only a very small portion of it (less than 1%) is present as the "biologically active" non-ionized amine. Most of the remaining phenylethylamine is bound to plasma protein or inside the erythrocytes.

Animals↗

PubMed1981

Simultaneous radioenzymatic determination of phenylethylamine, phenylethanolamine, tyramine and octopamine in plasma of patients with hepatic encephalopathy.

A sensitive radioenzymatic assay for the simultaneous determination of phenylethylamine, phenylethanolamine, tyramine and octopamine in plasma samples is reported. After extraction with ethanol, the amines are subjected to enzymatic N-methylation with labelled S-adenosylmethionine, preceded in the case of phenylethylamine and of tyramine, by an enzyme-catalyzed beta-hydroxylation step. The procedure is completed by extraction with toluene containing different amounts of isoamylalcohol, followed by controlled evaporation of the solvent. A generalized and highly significant increase in the concentration of all the four amines was found in plasma samples from patients suffering from hepatic encephalopathy.

Ethanolamines↗

PubMed1976

Does phenylethylamine cause schizophrenia?

The model psychosis associated with amphetamine overdosage is known to bear a close resemblance to acute paranoid schizophrenia. Amphetamine is chemically similar to the endogenous sympathomimetic amine, phenylethylamine, which possess many of its pharmacological properties. It is suggested that some cases of schizophrenia may be associated with an abnormal phenylethylamine response, either from increased concentrations of the amine or from abnormal receptor sensitivity to it.

Brain↗

PubMed1997

Metabolism of phenylethanolamines and 2-oxo-2-phenylethylamines in the rat.

1. The metabolism of a series of phenylethanolamines and 2-oxo-2-phenylethylamines was examined in vivo in the rat. 2. The urinary excretion of the corresponding mandelic acids was, in general, considerably greater for 2-oxo-2-phenylethylamines than for the corresponding phenylethanolamines. Of the putative metabolites of the former class of compounds only phenylglyoxals yielded mandelic acids.

Animals↗

PubMed1997

Effects of some phenylethylamines in rhesus monkeys trained to discriminate (+)-amphetamine from saline.

Although the structure-activity relationships (SAR) for the discriminative stimulus (DS) effects of phenylethylamines (PEAs) have been extensively evaluated in rats, only isolated components of the SAR have been studied in other species. Since DS effects in animals predict subjective effects in humans, it is important to establish cross-species generality of substitution results. In the present experiment, rhesus monkeys (n = 4) were trained to discriminate (+)-amphetamine (0.56 or 1.0 mg/kg, i.g.) from saline in a two-lever drug discrimination paradigm. Responding was maintained under a fixed-ratio discrete-trials schedule of shock avoidance. (+)-Amphetamine, and the N-substituted phenylethylamines (+)-methylamphetamine, and (+)-ethylamphetamine all engendered dose-dependent, full substitution for (+)-amphetamine and had no effect on rate of responding. In contrast, the ring-substituted compounds (+/-)-4-methoxyamphetamine (PMA), (+/-)-2,5-dimethoxy-4-methylamphetamine (DMA), (+/-)-2,5-dimethoxy-4-methylamphetamine (DOM), and (+/-)-3,4, 5-trimethoxyamphetamine (TMA) occasioned little or no (+)-amphetamine-appropriate response up to doses of 3.0 or 10 mg/kg. Therefore, it appears that monkeys respond to N-substituted amphetamines in the same way as rats, at least qualitatively. Considering that ring-substituted compounds have been found to partially substitute for (+)-amphetamine in rats, it is possible that the (+)-amphetamine DS may be pharmacologically more selective in monkeys. However, methodological differences may also explain differences between experiments.

Amphetamine↗

PubMed2000

Computer-aided design, synthesis and biological assay of p-methylsulfonamido phenylethylamine analogues.

Class III antiarrhythmic agents selectively delay the effective refractory period (ERP) and increase the transmembrance action potential duration (APD). Based on our previous studies, a set of 17 methylsulfonamido phenylethylamine analogues were investigated by 3D-QSAR techniques of CoMFA and CoMSIA. The 3D-QSAR models proved a good predictive ability, and could describe the steric, electrostatic and hydrophobic requirements for recognition forces of the receptor site. According to the clues provided by this 3D-QSAR analysis, we designed and synthesized a series of new analogues of methanesulfonamido phenylethylamine (VIa-i). Pharmacological assay indicated that the effective concentrations of delaying the functional refractory period (FRP) 10ms of these new compounds have a good correlation with the 3D-QSAR predicted values. It is remarkable that the maximal percent change of delaying FRP in microM of compound VIc is much higher than that of dofetilide. The results showed that the 3D-QSAR models are reliable.

Animals↗

PubMed1998

Exploring a channel to the active site of copper/topaquinone-containing phenylethylamine oxidase by chemical modification and site-specific mutagenesis.

Copper amine oxidase contains an organic redox cofactor, 2,4, 5-trihydroxyphenylalaninequinone (topaquinone, TPQ), derived by the post-translational modification of a specific tyrosyl residue. To identify amino acid residues participating in the biogenesis of TPQ in the recombinant phenylethylamine oxidase from Arthrobacter globiformis, we have modified the copper/TPQ-less apoenzyme and the copper/TPQ-containing holoenzyme with 4-fluoro-7-nitrobenzo-2-oxa-1, 3-diazole (NBD-F). In the apoenzyme modification, the Cu2+-dependent, self-processing formation of the TPQ cofactor was retarded in accordance with the amount of NBD incorporated. The holoenzyme was also rapidly inactivated by incubation with NBD-F. The inactivation was prevented almost completely in the presence of an oxidation product from phenylethylamine, phenylacetaldehyde. Furthermore, the reaction of an inhibitor, phenylhydrazine, with TPQ was much slower in the NBD-labeled holoenzyme than in the native holoenzyme. Sequence analysis of the NBD-labeled holoenzyme has identified Lys184 and Lys354 as the labeled sites. The two Lys residues are located close to the entrance to a channel, which has been found by recent X-ray crystallographic studies to be suitable for the movement of substrates and products to and from the Cu2+/TPQ-active site buried in the protein interior (Wilce, M. C. J., et al. (1997) Biochemistry 36, 16116-16133). However, site-specific mutant enzymes for Lys184, Lys354, and the neighboring invariant His355 had normal capacities for the TPQ formation in apoenzyme. These residues were also found to be dispensable for catalytic activity of holoenzyme. Thus, modification of Lys184 and Lys354 with NBD-F presumably causes structural perturbations of the substrate channel or steric hindrance for the access of small molecules to the active site through the channel.

4-Chloro-7-nitrobenzofurazan↗

PubMed1976

Phenylalanyl transfer ribonucleic acid synthetase from Escherichia coli B. Potent inhibition by analogues of N-benzyl-2-phenylethylamine.

A potent new class of inhibitors of phenylalanyl-tRNA synthetase from Escherichia coli B is described. N-Benzyl-2-phenylethylamine is a competitive inhibitor with respect to L-phenylalanine and appears to possess the structural features required for near-optimal binding. Hydrophobic substituents at the ortho position of either ring appear to be well tolerated, but substituents on both rings lead to large losses in binding. Poor noncompetitive inhibitors resllt from alkylation of the secondary nitrogen, further separation of the N-benzyl group from the nitrogen, or alkylation at the alpha position of the N-benzyl moiety. In contrast, placement of a methyl group at the 1 position of the 2-phenylethylamine moiety to give N-benzyl-D-amphetamine results in the most potent inhibitor yet described for this enzyme.

Amino Acyl-tRNA Synthetases↗

PubMed1987

2-Phenylethylamine catabolism by Escherichia coli K12.

Escherichia coli K12 grows on 2-phenylethylamine as sole carbon and energy source by converting it, via phenylacetaldehyde, to phenylacetic acid. Phenylacetaldehyde was formed by the action of an inducible amine oxidase and catalase activity was increased sixfold, presumably to ensure removal of the H2O2 that was expected to be a product of the amine oxidation. The phenylacetaldehyde was oxidized to phenylacetic acid by an inducible NAD+-dependent dehydrogenase. Mutants defective in phenylacetaldehyde dehydrogenase cannot grow on 2-phenylethylamine as carbon and energy source but can still use it as a nitrogen source.

Aldehyde Oxidoreductases↗

PubMed1985

Prevention of dopaminergic toxicity of MPTP in mice by phenylethylamine, a specific substrate of type B monoamine oxidase.

N-methyl-4-phenyl-1,2,5,6-tetrahydropyridine (MPTP) is toxic to dopaminergic neurones in several mammalian species including mice. Combined treatment with phenylethylamine prevented in mice the long-term (30 days post-treatment) dopamine depletions in striatum induced by MPTP. Phenylethylamine, a naturally-occurring specific substrate of monoamine oxidase (MAO) type B, probably protects against effects of MPTP by competitively inhibiting the oxidative conversion of MPTP to its toxic metabolite N-methyl-4-phenylpyridinium ion catalysed by MAO-B.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed2005

Effects of beta-phenylethylamine on dopaminergic neurons of the ventral tegmental area in the rat: a combined electrophysiological and microdialysis study.

The effects of systemic administration of beta-phenylethylamine (beta-PEA) and microiontophoretically applied beta-PEA on the spontaneous discharge of dopamine (DA) neurons in the ventral tegmental area (VTA) of the anesthetized rat were examined. Intravenous administration of beta-PEA (1.0, 2.5, and 5.0 mg/kg) and microiontophoretic applications of beta-PEA caused inhibitory responses in DA neurons. Systemic administration and microiontophoretic applications of beta-PEA induced dose- or current-dependent responses. The systemic beta-PEA-induced inhibitory responses were reversed by pretreatment with the DA D(2) receptor antagonists haloperidol (0.5 mg/kg i.p.) and sulpiride (10 mg/kg i.p). Pretreatment with reserpine (5 mg/kg i.p. 24 h earlier) did not completely block the systemic administration of beta-PEA (2.5 mg/kg) inhibition. A microdialysis study of freely moving rats demonstrated that the extracellular DA level increased significantly in response to local application of beta-PEA (100 muM) in the VTA via a microdialysis probe, and local application of beta-PEA-stimulated somatodendritic DA release in the VTA. The beta-PEA-induced release of DA was calcium ion-independent and was enhanced by pretreatment with pertussis toxin. These findings indicate that beta-phenylethylamine inhibits DA neuron activity via DA D(2) autoreceptors in the rat VTA and that this inhibitory effect is mediated by the somatodendritic DA release.

Animals↗

PubMed1982

(+)-Amphetamine binding to rat hypothalamus: relation to anorexic potency for phenylethylamines.

Saturable and stereospecific binding sites for (+)-[3H]amphetamine were demonstrated in membrane preparations from rat brain. The density of these binding sites varies among brain regions and is highest in the hypothalamus and brainstem. Specific (+)-[3H]amphetamine binding in hypothalamus is largely confined to synaptosomal membranes, rapidly reversible, and sensitive to both heat and proteolytic enzymes. Scatchard analysis of the equilibrium binding data revealed two distinct sites with apparent affinity constants of 93 and 300 nanomoles per liter, respectively. The effects of various psychotropic drugs as well as a number of putative neurotransmitters and related agonists and antagonists in displacing specific (+)-[3H]amphetamine binding demonstrate that these binding sites are not associated with any previously described neurotransmitter or drug receptors, but are specific for amphetamine and related phenylethylamine derivatives. Furthermore, the relative affinities of a series of phenylethylamine derivatives for (+)-[3H]amphetamine binding sites in hypothalamic membranes is highly correlated to their potencies as anorexic agents. These results suggest the presence of specific receptor sites in hypothalamus that mediate the anorexic activity of amphetamine and related drugs.

Animals↗

PubMed1993

An Alkalophilic Bacillus sp. Produces 2-Phenylethylamine.

A large amount of 2-phenylethylamine was produced in cells of alkalophilic Bacillus sp. strain YN-2000. This amine is secreted in the medium during the cell growth. The amounts of 2-phenylethylamine in both cells and medium change upon changing the pH of the medium.

Journal Article↗

PubMed2001

Phenylethylamine, a possible link to the antidepressant effects of exercise?

OBJECTIVES: To determine in this pilot study whether aerobic exercise affects phenylacetic acid concentration in the urine. METHODS: Twenty healthy men provided 24 hour urine samples on two consecutive days for the determination of phenylacetic acid levels. Before and during day 1, subjects refrained from physical activity; on day 2 subjects ran on a treadmill at 70% of their maximal heart rate reserve (MHRR) for 30 minutes. RESULTS: The 24 hour mean urinary concentration of phenylacetic acid was increased by 77% after exercise. CONCLUSION: As phenylacetic acid concentration in urine reflects phenylethylamine level, which is known to have antidepressant effects, phenylethylamine may be linked to the therapeutic effects of physical exercise on depression.

Adolescent↗