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PubMed1986

[Phenylethylamine fluorides. II. Synthesis and neurobiochemistry in the rat].

Sixteen fluorinated phenylethylamines analogous to catecholamine were obtained by fluoration from the corresponding amino-alcohols. The biological activity of the compounds was evaluated by determining their affinity for the central adrenergic receptors of rat brain membranes and by measuring the monoamine synaptosomal uptake. These compounds significantly inhibited serotonine uptake, but they showed no affinity for amphetaminergic binding sites.

Animals↗
PubMed1985

Trace amines inhibit the electrically evoked release of [3H]acetylcholine from slices of rat striatum in the presence of pargyline: similarities between beta-phenylethylamine and amphetamine.

Amphetamine (AMPH) inhibits the electrically evoked release of [3H]acetylcholine (ACh) from rat striatal slices through the activation of inhibitory dopamine receptors. Naturally occurring analogs of amphetamine (AMPH) such as beta-phenylethylamine (beta-PEA), tyramine (TYR) and octopamine (OCT) are present in trace amounts in the brain of several species. We have studied in this model, in comparison with AMPH, the effects of beta-PEA, TYR and OCT, in order to explore if their central effects are mediated through an action involving dopaminergic nerve terminals or whether they activate a specific receptor directly. In contrast to the results obtained with AMPH, in the absence of inhibition of monoamine oxidase activity, the three amines beta-PEA (0.1-10 microM), TYR (0.1-10 microM) and OCT (10 microM) did not affect the electrically evoked release of [3H]ACh. On the other hand, in the presence of pargyline (10 microM), the three amines inhibited the electrically evoked release of [3H]ACh and all subsequent experiments were carried out in the presence of pargyline. After pretreatment with reserpine (5 mg/kg s.c., 24 h), which results in a 95% depletion of the endogenous dopamine content, OCT lost its inhibitory effect on [3H]ACh release, whereas beta-PEA and TYR still inhibited the electrically evoked release of [3H]ACh. Reserpine pretreatment (5 mg/kg s.c., 24 h) combined with alpha-methyl-p-tyrosine (300 mg/kg i.p., 2 h) reduced endogenous dopamine levels by 99.9%, but, under these conditions, beta-PEA, TYR and AMPH still retained their inhibitory effect on [3H]ACh, release. These inhibitory effects of beta-PEA and AMPH on [3H] ACh release were antagonized by S-sulpiride (0.1 microM). In striatal slices from untreated rats, the inhibition of [3H]ACh released by beta-PEA (30 microM), TYR (30 microM) or AMPH (10 microM) was abolished completely after a 6-hydroxydopamine lesion of the nigro-striatal dopaminergic system. The present data indicate that in order to inhibit the release of [3H]ACh from rat striatal slices in vitro, OCT requires the integrity of vesicular stores of dopamine. On the other hand, beta-PEA, TYR and AMPH are still active when the dopamine levels are depleted, although they require the integrity of the dopaminergic nerve terminal. Inhibition of monoamine oxidase is essential to demonstrate the inhibitory effects of exogenous beta-PEA, TYR and OCT on cholinergic transmission. Our results indicate that a hypothesis concerning a possible physiopathological role of endogenous beta-PEA or TYR should involve concomitant changes in monoamine oxidase activity.

Acetylcholine↗
PubMed1986

Clinical studies on the phenylethylamine hypothesis of affective disorder: urine and blood phenylacetic acid and phenylalanine dietary supplements.

To test the hypothesis that 2-phenylethylamine (PEA) modulates affect, plasma levels and urinary excretion of its main metabolite, phenylacetic acid (PAA), were studied in depressed and manic subjects, and the mood-elevating effects of its precursor, L-phenylalanine, were studied in depressed subjects. Mean total plasma PAA concentrations were 491.83 +/- 232.84 ng/ml in 12 healthy volunteers and 300.33 +/- 197.44 ng/ml in 23 drug-free patients with major depression. The 24-hour urinary PAA excretion was also measured in 48 healthy volunteers (141.1 +/- 10.2 mg PAA/24 hr) and in 144 patients with major depression (78.2 +/- 41.0 mg PAA/24 hr). The results suggest that low plasma and urinary PAA may be state markers for depression and are compatible with the PEA hypothesis. In further support, phenylalanine elevated mood in 31 of 40 depressives.

Adult↗
PubMedDate not supplied

[Differences and similarity in the interaction of fenibut, baclofen and diazepam with phenylethylamine].

The derivatives of GABA and beta-phenylethylamine (PEA) the tranquilizer phenibut and muscle relaxant baclofen (p-chloro-beta-phenyl-GABA, lioresal) diminished all studied effect of PEA in mice, namely seizures, sedation, excitation, hyperthermia. Diazepam diminished only seizures whereas haloperidol excitation and hyperthermia. PEA injections anatogonized (the sedative and hypothermic effects of phenibut and diazepam and the anticonvulsant (against l-kynurenine) effect of phenibut and baclofen. The role of antagonism to PEA in the mechanism of the antianxiety effect of tranquilizers is discussed.

Animals↗
PubMed1979

[Effect of beta-phenylethylamine on evoked potentials of the neostriatum of rats].

The effect of intraperitoneal (70 mg/kg) and local (39 ug) administration of beta-phenylethylamine (beta-PEA) on evoked potentials (EP) in the caudate nucleus upon stimulation of substantia nigra zona compacta (SNC) and frontal cortex in rats has been studied. beta-PEA, glutamate and haloperidol were injected into the caudate nucleus by means of a system consisting of a pushpull cannule and an electrode for simultaneous registration of EP. Specificity in the effect of the drugs on EP in response to stimulation of the cortex and substantia nigra was revealed. The intraperitoneal injection of beta-PEA induced, comparatively to the application, more rapid and potent decrease in the amplitude of the component (N2-P2) as a result of the substantia nigra stimulation and slightly influenced the EP amplitude in stimulation of the frontal cortex. It was established using haloperidol that the component (N2-P2) of EP in response to the substantia nigra stimulation is of dopaminergic neuron function in the nigro-neostrital system of the rat brain.

Animals↗
PubMed1979

Effects of the oestrous cycle and exogenous ovarian steroids on metabolism of beta-phenylethylamine in rat lung.

1 Metabolism of [14C]-beta-phenylethylamine (PEN), a substrate for monoamine oxidase-B (MAO-B), was measured in lung homogenates and in perfused lungs during the 4 day oestrous cycle of the rat. 2 Metabolism in vitro was high during met-oestrus and di-oestrus and low during pro-oestrus and oestrus; this variation in activity correlated with changes in Vmax of the enzyme without changes in Km. 3 PEN metabolism in lung homogenates was also altered by treatment of rats with 17 beta-oestradiol but not by progesterone treatment. 4 Metabolism of [14C]-PEN in perfused lungs was the same during either pro-oestrus or met-oestrus. Uptake of [14C]-PEN in perfused lung measured directly was also the same at these two stages. 5 These results demonstrate that in lungs MAO-B activity was affected by endogenous changes in steroid level but that such changes in enzymic activity were not reflected in the metabolic properties of whole lung.

Animals↗
PubMed1984

[Presynaptic regulation of dopamine release by beta-phenylethylamine].

Experiments with local perfusion of the rat neostriatum and subsequent chromatography of the perfusate have shown that addition of beta-phenylethylamine (beta-PEA) to the perfusion medium in a concentration of 10(-3) M enhanced spontaneous and inhibited the K+-induced release of 3H-dopamine preliminarily applied to the neostriatum. The stimulating effect of beta-PEA was Ca2+-dependent and was potentiated in sodium-free media. The inhibitory effect of beta-PEA on the K+-induced release of 3H-DA was abolished by haloperidol, a blocker of dopamine receptors. This fact allows one to suggest that this effect of beta-PEA is mediated by presynaptic dopamine autoreceptors. The data obtained indicate that beta-PEA can modulate the dopaminergic synaptic transmission depending on functional activity of dopaminergic neurons.

Animals↗
PubMed1980

[Effect of beta-phenylethylamine on synaptosomal and glial transport of labeled neuromediators].

The effect of beta-phenylethylamine (beta-PEA) on the accumulation of 14C-serotonin, 14C-glutamate and 3H-gamma-aminobutyric acid (3H-GABA) by synaptosomes of the caudate nucleus and cerebral cortex of rats and rabbits was studied for the first time. beta-PEA inhibits 14C-serotonin influx and exerts no material effect on 14C-glutamate and 3H-GABA uptake. beta-PEA inhibits the synaptosomal and glinal accumulation approximately to the same extent. The data obtained are in good agreement with the concepts of the regulatory role of beta-PEA in the transport of biogenic monoamines in the nerve ending membranes. A similarity of the inhibitory effects of beta-PEA to those of amphetamine is suggested.

2-Hydroxyphenethylamine↗
PubMedDate not supplied

Effect of prolonged desmethylimipramine administration on the pulmonary clearance of 5-hydroxytryptamine and beta-phenylethylamine in rats.

Monoamine oxidase (MAO) is responsible for the pulmonary metabolism of 5-hydroxytryptamine (5-HT) and phenylethylamine (PEA). In the present study the effects of treatment of rats with the tricyclic antidepressant desmethylimipramine (DM) on the disposition of 5-HT and PEA in isolated perfused rat lungs was investigated. DMI accumulation in the lung reached a plateau after 6 days of treatment with mean values of 1.1, 6.1, and 315 nmol/lung at dose levels of 0.67, 6.7, and 33 mumol/kg/day, respectively. During a 10-min perfusion at a concentration of 10(-6) M, both 5-HT and PEA were rapidly taken up and extensively metabolized by lungs from control animals. DMI treatment decreased pulmonary clearance of 5-HT and the extent of its metabolism in a partially dose-related manner. Efflux experiments showed that no unmetabolized 5-HT appeared in the effluent from lungs of either control or DMI-treated rats. These data suggest that DMI decreases both transport of 5-HT across the pulmonary endothelium and MAO activity. PEA clearance in perfused lung was decreased in a dose-related manner by DMI treatment with a corresponding decrease in its metabolism. In efflux experiments, unmetabolized PEA was only found in the perfusate from lungs of DMI-treated rats. It was concluded that PEA clearance after DMI results almost entirely from inhibition of pulmonary MAO. The data also suggest that there may be two discrete pools of MAO in lung, one of which is relatively unaffected by DMI.

Animals↗
PubMed1977

Mass fragmentographic demonstration of low amounts of beta-phenylethylamine in human urine.

beta-Phenylethylamine (PEA) is determined with a simple, rapid and highly specific assay, 5 ml human urine, using GLC combined with mass fragmentography. The 24 h urinary excretion of PEA in ten healthy male subjects ranged from 28 to 131 nmol/24 h with a mean (+/- SD) of 66 (+/- 9) nmol/24 h. It is concluded that reinvestigation of PEA-excretion in psychiatric patients is needed, since earlier less specific methods have measured much higher levels of PEA in human urine.

Chromatography, Gas↗
PubMed1983

Comparison of central actions of intraventricularly administered octopamine, phenylethylamine and adrenaline in rats.

The paper reviews and summarizes the results obtained in a series of experimental papers on the central action of octopamine (OCT), phenylethylamine (PEA) and adrenaline (ADR) on the central nervous system. The mechanism of amines' central action is related to stimulation of noradrenergic and dopaminergic systems. The central effect of OCT and PEA seems to be related to the interaction with specific binding sites.

Animals↗
PubMed1983

Comparison of the effects of beta-phenylethylamine and d-amphetamine on rat isolated atria.

beta-Phenylethylamine (PEA) produced a positive chronotropic effect in the spontaneously beating isolated rat atria. The concentration-response curves to PEA and to d-amphetamine (AMPH) were virtually superimposed and potentiated to the same extent by inhibition of monoamine oxidase with pargyline. As reported for AMPH, the rate accelerating effect of PEA was abolished by pretreatment with reserpine. In the reserpinized tissue, the responses to PEA were partly restored by pargyline pretreatment and fully restored after the incubation with norepinephrine (NE). Repeated exposures to high concentrations of both PEA and AMPH produced tachyphylaxis to low concentrations of the amines but did not modify the endogenous atrial content of NE. in atria labeled with [3H]NE, PEA (6.4 microM) and AMPH (7.9 microM) increased the overflow of tritium mainly as unmetabolized [3H] NE (90%). For both drugs the increase in 3H-transmitter outflow coincided with the positive chronotropic response and it was independent on external Ca++. Cocaine (3.3 microM), which inhibits the uptake mechanism of catecholamines, displaced to the right the concentration-response curves to both PEA and AMPH and reduced the overflow of [3H]NE elicited by either amine. The release of 3H-products elicited by PEA was not modified by drugs that inhibit the uptake mechanism of NE accumulation, such as 26 microM corticosterone or 28 microM hydrocortisone. The results presented show that PEA behaves as AMPH as far as the mechanism of their indirect sympathomimetic effect is concerned. If accepted that PEA and AMPH, due to their high lipid solubility, might freely diffuse into nerves, the antagonism caused by cocaine on the effects of both amines could be interpreted as being the result of the inhibition by this drug of the carrier-mediated efflux of NE.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1983

[Effect of beta-phenylethylamine on locomotor activity and brain catecholamine metabolism in mice].

beta-Phenylethylamine (PEA) is a naturally occurring compound and its structure is close to amphetamine. The effects of PEA on locomotor activity and brain catecholamine metabolism in mice were investigated. Mice were injected with PEA 50 mg/kg intraperitoneally. PEA produced increased locomotor activity between 3 and 6 min, then a decline to 20 min after the injection. There was decreased activity with a slight stereotyped behavior consisted of sniffing and head bobbing between 15 and 20 min. 3-Methoxy-4-hydroxy-phenylethyleneglycol (MHPG), homovanillic acid (HVA) and 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the whole brain were examined. MHPG levels showed no remarkable changes at 5 min after PEA, then increase at 30 and 60 min. HVA level was increased but DOPAC level was decreased at 60 min. Type B monoamine oxidase activity showed no remarkable changes in discrete regions of the brain at 5 and 30 min. These results suggest that PEA may not only release catecholamines but inhibit the reuptake of neurogenically released dopamine.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

A rapid and sensitive gas chromatographic method for quantitation of 2-phenylethylamine in brain tissue and urine.

A rapid, sensitive procedure for analysis of 2-phenylethylamine in brain tissue and urine is described. The method involves extraction with a liquid ion exchanger, elution with HCl, acetylation under aqueous conditions, pentafluorobenzoylation under anhydrous conditions and analysis using a gas chromatograph equipped with a capillary column and an electron-capture detector.

Animals↗
PubMed1980

Monoamine oxidase inhibitors potentiate phenylethylamine effects in rhesus monkeys.

Acute pretreatment with either a Type A monoamine oxidase inhibitor (MAOI), clorgyline, or a Type B MAOI, pargyline, markedly reduced the dose of phenylethylamine (PEA) required to produce checking and a variety of other behavioral changes in rhesus monkeys. Doses of PEA (5 or 10 mg/kg) which previously were without effect, now produced significant behavioral changes in pretreatment animals.

Animals↗
PubMed1981

The effect of intraventricular phenylethylamine and octopamine on the central effects of tremorine and pilocarpine and the acetylcholine level in the rat brain.

Phenylethylamine (PEA, 50 and 100 microgram ivc) and octopamine (OCT, 50 and 250 microgram ivc) potentiated the tremorine (10 mg/kg ip) induced hypothermia in the rat. This effect was partially antagonized by atropine (10 mg/kg ip). PEA and OCT significantly prolonged the duration of pilocarpine (100 mg/kg iv) induced catalepsy in rats. PEA (100 microgram ivc) and OCT (250 microgram ivc) depressed the acetylcholine (ACh) level in the cerebral cortex and striatum but did not affect it in the hippocampus. In addition, these amines enhanced the synthesis of ACh in the cerebral cortex, and PEA also in the rat striatum.

Acetylcholine↗
PubMed1982

The effect of intracerebroventricularly administered octopamine, phenylethylamine and epinephrine on the central serotonergic system of the rat.

Octopamine (OCT, 50-250 micrograms) and epinephrine (EPI, 10-100 micrograms) given intracerebroventricularly (icvtr) antagonized the head twitch response induced in the rat by 5-hydroxytryptophan or 5-methoxytryptamine, and hyperthermia induced by quipazine in rats kept at high ambient temperature. Phenylethylamine [PEA, 10-100 micrograms] did not change the action of serotonergic stimulants. OCT, PEA and EPI significantly depressed the cerebral level of serotonin [5-HT], and OCT also reduced the concentration of 5-hydroxyindoleacetic acid. OCT depressed, while EPI slightly accelerated the 5-HT turnover rate; PEA practically did not affect the turnover. The results indicate that OCT and EPI given icvtr to rats antagonize the central serotonergic system.

5-Hydroxytryptophan↗