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PubMedDate not supplied

Effects of amphetamine and phenylethylamine on catecholamine release in the glomerular layer of the rat olfactory bulb.

In the present work, we have shown electrochemically that in the rat olfactory bulb (OB), extracellular dopamine (DA) was highest in the glomerular layer (GL), whereas extracellular noradrenaline (NA) appeared to be more uniformly distributed across layers. The GL catecholamine (CA) responses to amphetamine (AMPH) and phenylethylamine (PEA) were also characterized electrochemically using an in vivo model. Results of this investigation show that at a lower dose (1 mg/kg), PEA had no effect on CA release. In contrast, at a higher dose (10 mg/kg), it produced similar increases in either extracellular DA (17.5 +/- 7%) or extracellular NA (14 +/- 3%), and DA exhibited dose-independent increases to AMPH (93 +/- 8%: 1 mg/kg vs. 97 +/- 6%: 10 mg/kg) whereas NA exhibited dose-dependent increases to AMPH (24.5 +/- 6%: 1 mg/kg vs. 39 +/- 7%: 10 mg/kg). These data indicate that (i) PEA may increase CA release but less efficiently than AMPH. (ii) AMPH is more efficient on the DAergic than on the NAergic system since AMPH-induced DA release exceeded 2-4 times the AMPH-induced NA release.

Amphetamine↗

PubMed1983

Phenylethylamine-like properties of baclofen.

Baclofen therapy resulted in improvement of dyskinesias only in patients with trunkal tardive dyskinesia. However, the appearance of undesirable side effects did not warrant continuation of treatment with this drug. Baclofen did not have any therapeutic effect in schizophrenia and moreover a trend towards a worsening of the psychiatric conditions with irritability, assaultiveness and prominent auditory hallucinations was observed. The effects of baclofen on tardive dyskinesia and schizophrenia can be explained in terms of its phenylethylamine-like properties.

Adult↗

PubMed1978

The effects of phenylethylamine in rhesus monkeys.

In controlled experiments rhesus monkeys that had received phenylethylamine (PEA) demonstrated behavior similar to that reported after the administration of amphetamines, except that tolerance to PEA did not develop. These findings are of psychiatric interest because PEA is found in the human body and is a specific substrate for type B MAO, which is found in decreased quantities in certain schizophrenic patients.

Amphetamine↗

PubMed1979

Phenylethylamine in rhesus monkeys: interactions with alpha-methyl-para-tyrosine and l-dopa.

Rhesus monkeys, pretreated with alpha-methyl-para-tryosine (AMPT) and subsequently injected with phenylethylamine (PEA), did not demonstrate the characteristic amphetamine-like PEA effects. However, when AMPT pretreatment was followed with l-dopa and then PEA injection, PEA effects were restored. These results are compatible with a dopamine theory of schizophrenia.

Animals↗

PubMed1991

Neuropsychological performance and urinary phenylethylamine in Tourette's syndrome.

Patients with Tourette's syndrome (TS) were grouped on the basis of levels of urinary phenylethylamine (PEA). These groups of TS patients were compared on an extensive battery of neuropsychological measures converted to age-corrected T scores based on published normative data. Patients with PEA levels below that of normal controls performed significantly worse than TS patients with normal PEA levels. The data were interpreted to suggest that abnormalities in PEA may contribute to neuropsychological deficits. Furthermore, these data may provide further support for an etiological subgroup of TS patients characterized by an abnormality in PEA metabolism. These data are discussed in regard to directions for further investigation.

Adolescent↗

PubMed1995

Phenylethylamine modulation of affect: therapeutic and diagnostic implications.

A review of the literature indicates that brain phenylethylamine (PEA) may be a neuromodulator of aminergic synapses and that it promotes energy, elevates mood, and favors aggression. Phenylacetic acid, the main metabolite of PEA, is decreased in the biological fluids of depressed subjects and schizophrenic subjects and is increased in schizoaffective subjects. The administration of PEA or of its precursor L-phenylalanine improves mood in depressed patients treated with a selective monoamine oxidase B inhibitor. The authors speculate that studies of PEA metabolism may have diagnostic value and that PEA administration may be therapeutic in selected depressed patients.

Affect↗

PubMed2005

Beta-phenylethylamine stimulates striatal acetylcholine release through activation of the AMPA glutamatergic pathway.

Using an in vivo intra-striatal microdialysis technique, we examined the effects of systemically administered beta-phenylethylamine (beta-PEA), a psychomotor stimulating trace amine, on striatal acetylcholine release in freely moving rats. Infusion of N-methyl-D-aspartic acid (NMDA; 10(-5) M) significantly increased acetylcholine release. In addition, locally applied amino-3-hydroxy-5-methylisozasole-4-propionic acid (AMPA; 10(-5) M) significantly increased acetylcholine release in the striatum. Intra-striatal application of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10(-5) M), an AMPA-type glutamatergic receptor antagonist, had little effect on acetylcholine release, while application of MK-801 (10(-5) M, 10(-6) M), an NMDA-type glutamatergic receptor antagonist, significantly reduced acetylcholine release. Acetylcholine within striatal perfusate was significantly increased by intraperitoneal administration of beta-PEA in a dose-dependent manner. This increase in acetylcholine release was completely blocked by application of CNQX (10(-5) M) through the microdialysis probe into the striatum. However, increased acetylcholine response to systemic beta-PEA was unaltered by addition of MK-801 to the perfusion medium. These results suggest a regulatory function of beta-PEA, mediated by AMPA-type glutamatergic receptors, on the release of acetylcholine in the rat striatum.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1989

Enhancement of spinal monosynaptic reflexes with phenylethylamine and related drugs through descending noradrenergic neurons.

The effects of phenylethylamine (PEA) and related drugs, such as methamphetamine, phenelzine, methylphenidate, nomifensine and mazindol on the spinal monosynaptic reflex (MSR) were investigated in rats treated with 6-hydroxydopamine (6-OHDA) or 5,6-dihydroxytryptamine (5,6-DHT). PEA (1 x 10(-5) mol/kg, i.v.) increased the amplitude of MSR in control rats, but decreased the amplitude in rats treated with 6-OHDA. Although PEA-related drugs increased the amplitude of MSR, they did not change the MSR amplitude in 6-OHDA-treated rats. In 5,6-DHT-treated rats, PEA-related drugs increased the amplitude of MSR, whereas PEA produced a decrease. These results support our previous suggestion that the enhancement of MSR by these drugs might be mediated through release of noradrenaline or inhibition of noradrenaline uptake at the noradrenergic synapses.

5,6-Dihydroxytryptamine↗

PubMed1989

Structure-activity relationships of phenylethylamine analogs in their serotonergic depressant effects on the spinal monosynaptic reflex in rats.

The effects of 2-phenylethylamine (PEA) and related compounds on the spinal monosynaptic reflex (MSR) were examined using C1-spinalized rats. At low doses, PEA, S(+)-amphetamine, S(+)-methamphetamine and phentermine increased the amplitude of the MSR, whereas high doses of these drugs reduced it. p-Substituted PEA analogs (p-C1-PEA, p-methoxy-PEA and (+/-)-p-C1-amphetamine) only reduced the MSR. Low doses of PEA-related rigid compounds, R(+)-2-aminotetralin, (+/-)-N-methyl-2-aminotetralin and (+/-)-N,N-dimethyl-2-aminotetralin only reduced the MSR. S(-)-2-Aminotetralin did not affect the MSR. Depressions of MSR produced by PEA, S(+)-methamphetamine and R(+)-2-aminotetralin were antagonized by ketanserin and haloperidol which have 5-hydroxytryptamine (5-HT) antagonistic activity, and the MSR depression caused by S(+)-methamphetamine but not PEA and R(+)-2-aminotetralin was abolished by intracisternal 5,6-dihydroxytryptamine treatment or chronic spinal transection. These results suggest that PEA-related compounds cause MSR depression by direct and indirect 5-HT agonistic mechanisms, and support the proposal that the PEA moiety which exists in R(+)-2-aminotetralin is important for the direct 5-HT agonistic activity of some hallucinogens.

Animals↗

PubMed2000

Stereoselective reactions. XXXII. Enantioselective deprotonation of 4-tert-butylcyclohexanone by fluorine-containing chiral lithium amides derived from 1-phenylethylamine and 1-(1-naphthyl)ethylamine.

Enantioselective deprotonation of 4-tert-butylcyclohexanone was examined using 1-phenylethylamine- and 1-(1-naphthyl)ethylamine-derived chiral lithium amides having an alkyl or a fluoroalkyl substituent at the amide nitrogen. The lithium amides having a 2,2,2-trifluoroethyl group on the amide nitrogen are easily accessible in both enantiomeric forms, and were found to induce good enantioselectivity in the present reaction.

Amides↗

PubMed1991

2-phenylethylamine and methamphetamine enhance the spinal monosynaptic reflex by releasing noradrenaline from the terminals of descending fibers.

Experiments were performed on spinalized rats transected at C1. Intravenous administration of 2-phenylethylamine-HCl (PEA-HCl) (0.3 and 1 mg/kg, i.v.) and methamphetamine-HCl (MAP-HCl) (0.1 and 0.3 mg/kg, i.v.) increased the amplitude of the monosynaptic reflex (MSR). The increase of the MSR caused by PEA and MAP was antagonized by prazosin-HCl and abolished by the pretreatment with reserpine (i.p.) and 6-hydroxydopamine (intracisternally, 14 days previously). A dopamine D1 antagonist, SK&F 83566-HBr (0.01 mg/kg, i.v.), and a D2 antagonist. YM-09151-2 (0.3 mg/kg, i.v.), did not antagonize the increasing effects produced by PEA and MAP. An inhibitor of type-B monoamine oxidase, (-)deprenyl-HCl (1 mg/kg, i.v.), prolonged the effect of PEA but not that of MAP, suggesting that PEA alone, and not its metabolites, enhanced the MSR. These results suggest that PEA and MAP increase the amplitude of the MSR by releasing noradrenaline from the terminals of descending noradrenergic fibers, and that PEA, an endogenous trace amine, has a mechanism of action similar to that of MAP.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1991

Inhibitory effects of beta-phenylethylamine on photic-evoked potentials in the visual cortex of the cat.

We investigated the effects of beta-phenylethylamine (PEA) on photic-evoked potentials recorded from the cerebral cortex (visual cortex) in the anesthetized cat. The photic-evoked potential consisted of negative (N) and positive (P) components in the cerebral cortex, with peak times of 39.4 +/- 15.4 msec and 57.5 +/- 16.3 msec, respectively. Intravenous administration of PEA (6.5, 12.5 and 25 mg/kg) induced a dose-dependent decrease in the amplitude of the N component of photic-evoked potentials. PEA-induced decreases in the amplitude of photic-evoked potentials (at 12.5 mg/kg) were antagonized by yohimbine (2 mg/kg). Prazocin (2 mg/kg, i.v.) and propranolol (0.5 mg/kg, i.v.) did not change the PEA-induced decrease of photic-evoked potentials. Methysergide (2 mg/kg, i.v.), haloperidol (1 mg/kg, i.v.) and naloxone (0.5 mg/kg, i.v.) also failed to alter the inhibitory effect of PEA. Pretreatment with alpha-methyl-p-tyrosine or reserpine did not completely attenuate the PEA-induced decrease of photic-evoked potentials. According to these results, PEA inhibits the photic-evoked potentials in the visual cortex partially through the noradrenergic alpha 2-receptor.

Anesthesia↗

PubMed1991

The response to acoustic stimulation and the changes in brain amine levels after repeated administration of beta-phenylethylamine in rats.

Reverse tolerance to stereotyped behavior was induced after repeated administration of beta-phenylethylamine (PEA) (50 mg/kg, i.p., daily for 10 days) in rats. The reverse tolerance was maintained for at least 4 weeks after the last administration. We studied the effects of acoustic stimulation on locomotor activity 2 days and 4 weeks after withdrawal from PEA and measured the changes in brain monoamine levels 4 weeks after the withdrawal. Locomotor activity during acoustic stimulation was increased in the saline treated group, and this response was unaffected after repeated PEA treatment. Four weeks after withdrawal, significant increases in noradrenaline levels in the cerebral cortex and decreases in 5-hydroxytryptamine levels in the hypothalamus were found. The effects of acoustic stimulation on locomotor activity and the changes in brain monoamine levels were different from those of methamphetamine treatment obtained in our previous study. In conclusion, it may be suggested that the response to acoustic stimulation after repeated PEA administration in rats cannot be a model for abnormal responsiveness to environmental stimulation that is observed in chronic paranoid schizophrenics.

Acoustic Stimulation↗

PubMed2002

Phenylethylamine induces an increase in cytosolic Ca2+ in yeast.

Beta-phenylethylamine (PEA) induced an increase in cytosolic free calcium ion concentration ([Ca2+]c) in Saccharomyces cerevisiae cells monitored with transgenic aequorin, a Ca2+-dependent photoprotein. The PEA-induced [Ca2+]c increase was dependent on the concentrations of PEA applied, and the Ca2+ mostly originated from an extracellular source. Preceding the Ca2+ influx, H2O2 was generated in the cells by the addition of PEA. Externally added H2O2 also induced a [Ca2+]c increase. These results suggest that PEA induces the [Ca2+]c increase via H2O2 generation. The PEA-induced [Ca2+]c increase occurred in the mid1 mutant with a slightly smaller peak than in the wild-type strain, indicating that Mid1, a stretch-activated nonselective cation channel, may not be mainly involved in the PEA-induced Ca2+ influx. When PEA was applied, the MATa mid1 mutant was rescued from alpha-factor-induced death in a Ca2+-limited medium, suggesting that the PEA-induced [Ca2+]c increase can reinforce calcium signaling in the mating pheromone response pathway.

Calcium↗

PubMed2003

Stereochemistry of 2-phenylethylamine oxidation catalyzed by bacterial copper amine oxidase.

The stereochemical course of the reaction catalyzed by a copper amine oxidase from Arthrobacter globiformis has been investigated using 2-phenylethylamine stereospecifically deuterium-labeled at the C1 position. Measurements of deuterium content in the product, phenylacetaldehyde, by gas chromatography-mass spectrometry revealed stereospecific abstraction of the pro-S hydrogen during the enzymatic oxidation, as predicted from the structure modeling for the enzyme-bound substrate.

Acetaldehyde↗

PubMed1979

Phenylethylamine as a biochemical marker of tiger.

Pheromones of the tiger happen to be a mixture of amines which are "fixed" by lipids. One of these, found always in all the four tigers investigated, is phenylethylamine. This may be a biochemical marker at a species level.

Animals↗

PubMed1979

Glucocorticoid and mineralocorticoid pathways in two adrenocortical carcinomas: comparison of the effects of o,p'-dichlorodiphenyldichloroethane, aminoglutethimide and 2-p-aminophenyl-2-phenylethylamine in vitro.

The synthesis of glucocorticoids and mineralocorticoids in vitro was studied in an adrenocortical carcinoma after alblation from an 11.5-year-old boy. This patient had been unsuccessfully treated with high doses of o,p'-dichlorodiphenyldichloroethane (o,p'-DDD) and aminoglutethimide. These in-vitro results were compared with those obtained with another adrenocortical carcinoma removed from a 26-year-old woman who had received no preoperative treatment. The sensitivity of these adrenocortical carcinomas to o,p'-DDD, aminoglutethimide and 2-(p-aminophenyl)-2-phenylethylamine (SKF 12185) was investigated. Synthesis of cortisol (47%) and corticosterone (45%) in control incubations showed that 11 beta-hydroxylase activity was not affected by the treatment. This explains the raised level of plasma cortisol in the treated child. All three compounds inhibited both 11 beta-hydroxylase and 18-hydroxylase activities up to 95%, depending on the inhibitor. This study shows (a) an inhibitory effect of o,p'-DDD on the steroidogenesis of an adrenocortical carcinoma in vitro, an effect not previously reported in man or laboratory animals, and (b) the in-vitro efficacy of o,p-DDD and aminoglutethimide on corticosteroidogenesis by a carcinoma unresponsive to treatment in vivo. This discrepancy between data obtained in vivo and in vitro could possibly be explained by either an insufficient ratio of ingested dose: tumour mass, or a malabsorption of the drugs in this patient.

Adrenal Cortex Neoplasms↗

PubMed1998

Characterization of dimethylguanosine, phenylethylamine, and phenylacetic acid as inhibitors of Ca2+ ATPase in end-stage renal failure.

The activity of the plasma membrane Ca2+ ATPase of chronic renal failure patients is decreased by circulating inhibitors yet to be characterized. In this study, inhibitors of Ca2+ ATPase were isolated from ultrafiltrate of patients with end-stage renal failure. They were identified as dimethylguanosine, phenylethylamine, and phenylacetic acid by chromatography and mass spectrometry. Ca2+ ATPase activity was measured spectrophotometrically as the difference in hydrolysis of ATP in the presence and absence of Ca2+ with different concentrations of ATP and the isolated substances. All of the identified compounds are sufficiently lipophilic to penetrate the blood-brain barrier and to accumulate in cerebral tissue. The inhibitory effects of these agents were additive. The apparent K(m) values for ATP and Ca2+ were not altered by these substances, suggesting a noncompetitive mechanism of inhibition. In plasma of healthy subjects, the substances were not detectable. The Ca2+ ATPase inhibitors identified may play a role in the pathophysiology of end-stage renal failure and, potentially, in monitoring toxic effects on cellular Ca2+ metabolism in renal failure.

Adult↗