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PubMed2004

Distribution of two triamines, spermidine and homospermidine, and an aromatic amine, 2-phenylethylamine, within the phylum Bacteroidetes.

Cellular polyamines of the newly additional 19 species belonging to the class Bacteroides of the phylum Bacteroidetes were analyzed by HPLC to display polyamine distribution as a chemotaxonomic marker within the total 41 species. Three profiles, the presence of spermidine, the presence of homospermidine and the absence of both triamines, corresponded to their phylogenetical positions within the four families of the class. The occurrence of an aromatic amine, 2-phenylethylamine, extracted into cellular polyamine fraction, was also determined within the 121 species distributed within the phylum. This aromatic amine was found in Cellulophaga lytica, Cytophaga latercula, Tenacibaculum amylolyticum, Tenacibaculum martimum, Tenacibaculum mesophilum and Psychroflexus torquis belonging to the family Flavobacteriaceae of the class Flavobacteria, and Flexibacter flexilis and Microscilla marina belonging to the family Flexibacteraceae of the class Sphingobacteria.

Bacteroidetes↗
PubMed1999

Developmental aspects of cerebrospinal fluid levels of beta-phenylethylamine and it's role in pediatric neurological disorders.

To clarify the role of beta-phenylethylamine (PEA) in pediatric neurological disorders, we have measured the cerebrospinal fluid (CSF) levels of PEA in 12 children with aseptic meningitis--6 were in the acute phase and the other 6 were in the recovery phase--and 5 children with Rett Syndrome (RS). The findings were compared with those obtained from 13 age-matched children with leukemia as child controls and from 10 adults patients without any neurological symptoms and signs as control. In the control group, the CSF PEA level was negatively correlated with age until 200 months (17 years) old. The mean PEA levels in meningitis and RS were significantly lower than that of child controls (p < 0.03). The alteration in the CSF levels of PEA may be related to transient changes in the dopaminergic tone in aseptic meningitis and neurological impairment, especially in the dopaminergic neurons in RS.

Age Factors↗
PubMed2000

Plasma beta-phenylethylamine in Parkinson's disease.

Plasma beta-phenylethylamine (PEA) levels were determined in 27 patients with Parkinson's disease (PD) in order to evaluate its relation with the severity or clinical course of PD. The plasma PEA concentrations in PD patients were significantly lower (mean +/- SD, 862 +/- 554 pg/ml) than those in the control group (1765 +/- 790 pg/ml) (p < 0.0001). The concentrations of PEA in plasma did not correlate with Hoen and Yahr stage. However, in serial measurements of the PEA of 5 patients in the progressive group of the clinical course of PD, the plasma PEA levels revealed a downward trend after one or two years. On the other hand, in 3 patients of non-progressive group, the plasma PEA remained at the same level. This study suggests that plasma PEA level might reflect nigrostriatal degeneration in patients with PD.

Aged↗
PubMed1995

SAR studies of fluorine-substituted benzylamines and substituted 2-phenylethylamines as substrates and inactivators of monoamine oxidase B.

To test whether addition of electron-withdrawing substituents to good substrates of monoamine oxidase (MAO) will transform them into inactivators, a series of fluorine-substituted benzylamines and a series of substituted 2-phenylethylamines were synthesized and tested as substrates and inactivators of monoamine oxidase B. All of the compounds were substrates. None of the benzylamines was an inactivator, but several of the phenethylamines were. These results suggest that either stronger electron withdrawing character or additional stabilizing factors are needed to stabilize the hypothesized enzyme adduct.

Animals↗
PubMed2000

Decreased cerebrospinal fluid levels of beta-phenylethylamine in patients with Rett syndrome.

To clarify the mechanism of brain impairment in Rett syndrome, we measured the cerebrospinal fluid levels of beta-phenylethylamine (PEA) in 17 patients with Rett syndrome. Findings were compared with those obtained in age-matched controls and diseased controls. The cerebrospinal fluid level of PEA was significantly lower in patients with Rett syndrome than in the controls (31% of control values). The alteration in the cerebrospinal fluid level of PEA may reflect dopamine system impairment in Rett syndrome.

Adult↗
PubMed2000

Convenient synthesis of optically active 2,2,2-trifluoro-1-phenylethylamine.

Amination of aryl trifluoromethyl ketones with ammonium formate readily gave racemic 2,2,2-trifluoro-1-arylethylamines in good yields. Resolution of 2,2,2-trifluoro-1-phenylethylamine was carried out with the Pseudomonas fluorescens lipase via enantioselective alcoholysis of its chloroacetamide.

Journal Article↗
PubMed2002

[Decreased beta-phenylethylamine in urine of children with attention deficit hyperactivity disorder and autistic disorder].

beta-phenylethylamine (PEA), a biogenic trace amine, acts as a neuromodulator in the nigrostriatal dopaminergic pathway and stimulates the release of dopamine. To clarify the mechanism of neurochemical metabolism in attention deficit hyperactivity disorder (ADHD), we measured the urine levels of PEA using gas chromatography-chemical ionization-mass spectrometry. The urinary levels of 3-methoxy-4-hydroxyphenyl glycol (MHPG), homovanillic acid (HVA), and 5-hydroxy-indoleacetic acid (5-HIAA) were determined by high performance liquid chromatography. Urine samples were collected in a 24 hour period. Findings were compared with those obtained from controls (N = 15), children with ADHD (N = 15), and children with autistic disorder (AD) (N = 5). The mean urinary levels of MHPG, HVA, and 5-HIAA in the children with ADHD were not significantly different from those of the controls or those with AD, whereas PEA levels were significantly lower in children with ADHD (11.23 +/- 13.40 micrograms/g creatinine) compared with controls (56.01 +/- 52.18 micrograms/g creatinine). PEA and MHPG levels in children with AD (14.75 +/- 14.37 micrograms/g creatine, 1.10 +/- 0.61 micrograms/mg creatine, respectively) were significantly decreased compared to controls (MHPG, 2.2 +/- 0.9 micrograms/mg creatine). The decreased urine PEA in children with ADHD and AD may suggest a common underlying pathophysiology. The decreased urine MHPG in children with AD might indicate the existence of an alteration in central and peripheral noradrenergic function.

Analysis of Variance↗
PubMed1975

The effect of beta-phenylethylamine on temperature in mice and its possible mechanisms of action.

Beta-phenylethylamine on injection into mice (100 mg/kg i.p.) produces a marked hyperthermia which is followed by a prolonged hypothermia. The hyperthermic response was studied in this report. The hyperthermic response was inhibited by p-chlorophenylalanine, methysergide, cyproheptadine, alpha-methyl-tyrosine, propranolol, practolol, phenoxybenzamine, phentolamine, haloperidol, pimozide, protriptyline and desipramine. Lysergic acid diethylamide potentiated the response, while p-chloroamphetamine was without effect. While FLA-63 potentiated the response, disulfiram and reserpine were ineffective in preventing the hyperthermia. Nicotinic acid and prostaglandin E1 did not prevent PE induced hyperthermia. It was concluded from these results that PE induced hyperthermia in mice is blocked by agents that reduce the effective concentration of either DA or 5-HT in the central nervous system (by either synthesis inhibitors or receptor blockers). The involvement with catecholaminergic neurons at least was postulated to be a result of PE induced release of DA from DA neurons.

Animals↗
PubMed2002

The enigma of conditioned taste aversion learning: stimulus properties of 2-phenylethylamine derivatives.

The functional aversive stimulus properties of several IP doses of (+/-)-amphetamine (1.25-10 mg.kg-1), 2-phenylethylamine (PEA, 2.5-10 mg.kg-1, following inhibition of monoamine oxidase with pargyline 50 mg.kg-1) and phenylethanolamine (6.25-50 mg.kg-1) were measured with the conditioned taste aversion (CTA) paradigm. A two-bottle choice procedure was used, water vs. 0.1 % saccharin with one conditioning trial and three retention trials. (+/-)-Amphetamine and phenylethanolamine induced a significant conditioned taste aversion but PEA did not. (+/-)-Amphetamine and PEA increased spontaneous locomotor activity but phenylethanolamine had no effects on this measure. Measurement of whole brain levels of these drugs revealed that the peak brain elevation of PEA occurred at approximately 10 min whereas the peak elevations of (+/-)-amphetamine and phenylethanolamine occurred at approximately 20 min. The present failure of PEA to elicit conditioned taste aversion learning is consistent with previous reports for this compound. The differential functional aversive stimulus effects of these three compounds are surprising since they exhibit similar discriminative stimulus properties and both (+/-)-amphetamine and PEA are self-administered by laboratory animals. The present data suggest that time to maximal brain concentrations following peripheral injection may be a determinant of the aversive stimulus properties of PEA derivatives.

Amphetamine↗
PubMed1975

[Effects of beta-phenylethylamine derivatives on the central nervous system. (5) The effect of intracerebral administration of tyramine on head twitching in mice pre-treated with isocarboxazid].

Effects of drugs on head-twitches induced by tyramine (Ty) in isocarboxazide (Iso) pretreated mice were studied and the following results obtained: 1) In beta-phenylethylamine derivatives, p-hydroxyamphetamine in non-treated and Iso-pretreated mice and Ty in Iso-pretreated mice produced head-twitches. 2) Injection of 5-HTP (i.c. and i.p.) into mice induced head-twitches. 3) Although head-twitches were not induced by a low dose of 5-HTP (20 mg/kg, i.p.), in Iso pretreated mice, the number of headtwitches increased markedly in the Iso-Ty treated group when Ty was injected i.c. in Iso+5-HTP (20 mg/kg) pretreated mice. 4) When Iso-Ty was injected into alpha-methyl-p-tyrosine pretreated mice, the number of head-twitches increased markedly compared with Iso-Ty treated group. 5) When Iso-Ty was injected into mice sustained with p-chlorophenylalanine, the number of head-twitches decreased markedly compared with the Iso-Ty treated group. 6) The number of head-twitches decreased markedly when Iso-Ty was injected into dimetotiazine pretreated mice, however the administration of Iso-Ty in haloperidol pretreated mice had no influence on head-twitches. 7) It is concluded that serotonin is the acting mediator in the head-twitch response.

5-Hydroxytryptophan↗
PubMed1990

Attenuation of effects of phenylethylamine on social and individual behaviour in mice by ethanol pretreatment.

Beta-phenylethylamine (PEA, 10 mg/kg, intraperitoneally) exerts the following behavioural effects in mice: (1) a decrease in the rate and duration of contacts (sniffings), typical of anxiogens, in albino SHR (bred from Swiss) male mice and a decrease in the duration of contacts in C57l/6 mice; (2) a decrease in the duration of grooming in both strains; (3) an increase in locomotion and rearings in long-sleeping C57Bl/6 mice. Pretreatment with ethanol (100 mg/kg, orally) diminished these effects of PEA. It is suggested that the anxiolytic action of ethanol may be related to its antagonism of PEA.

Alcohol Drinking↗
PubMed1989

[beta-Phenylethylamine and amphetamine: similar aspects in their behavioropharmacological and neurochemical characteristics].

The authors found there was behavioral sensitization induced by repeated intermittent treatments with beta-phenylethylamine (PEA), an endogenous trace amine, similar to the so-called reverse-tolerance phenomenon which persists long after the withdrawal. A series of behavioropharmacological and neurochemical studies on the PEA-sensitized rats were compared with that on the sensitization induced by amphetamines (AMP). The major portion of this review focused on an involvement of dopaminergic modifications in the reverse tolerance caused by both PEA and AMP. The enhanced stereotype in the PEA-sensitized rats was found to be accompanied by augmentation of presynaptic dopaminergic activity in nigrostriatal and mesocorticolimbic systems by means of regional dissected and in vivo dialysis methods. In particular, a simultaneous measurement of endogenous PEA levels in striatum led us to speculate that the DA terminals in sensitized animals are hyperresponsive to PEA, resulting in enhanced DA release. D2 receptor bindings in nucleus accumbens, not in striatum, also altered in PEA-sensitized rats. In addition, recent literature concerning changes in PEA levels in body fluids in psychiatric disorders are summarized. Lastly, the attractive reports regarding the possibility that central actions of AMP would be mediated by endogenous PEA and that PEA is co-localized with DA in the same neurons were reviewed, suggesting an important role of endogenous PEA in generating the psychostimulant-induced and endogenous psychosis.

Amphetamine↗
PubMed1989

Effects of phenylethylamine on rat locomotor behavior and avoidance learning.

1. The effects of beta-phenylethylamine (PEA) alone and in association with caroxazone, a potent inhibitor of monoamine oxidase B (MAO B), on the activity and long-term memory in the wheel-shaped activity monitor and on fixed-interval two-way avoidance acquisition were studied in rats. In a separate study, we determined the effects of PEA and of d-amphetamine on the variable-interval two-way avoidance acquisition. 2. The action of PEA was markedly different from that of amphetamine in several aspects. The stimulating effects of PEA in the wheel-shaped activity monitor were of a more subtle nature than those of amphetamine and in the variable-interval two-way avoidance acquisition PEA had no effect, while amphetamine improved performance. 3. PEA did not induce an increase in path-choice stereotypy, but caroxazone did. The absence of any caroxazone-session interaction effects on the path iteration frequency suggested that there were no long-term memory effects. 4. In the fixed-interval two-way avoidance acquisition experiments, PEA increased the avoidance responses of rats while caroxazone had no effect. The association of the two drugs did not potentiate either.

Animals↗
PubMed1988

Determination of beta-phenylethylamine in catfish (Parasilurus asotus) tissues by gas chromatography/mass spectrometry.

1. beta-Phenylethylamine (PEA) was detected and quantitated in tissues of the catfish, Parasilurus asotus, by very specific and sensitive gas chromatography/mass spectrometry. 2. The selected ion monitoring was made with a strong quasi-molecular ion of the pentafluoropropionic derivative of PEA in the positive chemical ionization mode. 3. PEA was found in all tissues tested ranging from 2.8 to 38.2 ng/g wet wt tissue. It was highest in the spinal cord, followed by the skin, brain and intestine.

2-Hydroxyphenethylamine↗
PubMed1986

The effect of repeated administration of (-) deprenyl on the phenylethylamine-induced stereotypy in rats.

Phenylethylamine (PEA) in a dose of 40 mg/kg induces a moderate and short-lasting stereotype behaviour. The intensity and duration of PEA-induced stereotypy was strongly potentiated in rats with single selective doses of (-) deprenyl and J-508 (0.25 and 0.1 mg/kg s.c., respectively), which inhibit selectively the B form of MAO. Neither the increase of the single dose nor the daily administration of the selective doses of (-) deprenyl and J-508 for eight weeks caused a more intense or longer lasting potentiation of the PEA effect than single small dose of these drugs. Stopping administration of MAO-B inhibitors, normal sensitivity towards PEA returned after 3-4 weeks, in a parallel way with the recovery of MAO-B activity in the brain. Clorgyline, the selective inhibitor of MAO-A failed to influence the effect of PEA (0.25-2 mg/kg s.c.). The data support the view that the strong potentiation of the stimulatory effects of endogenous PEA via inhibition of its metabolism by (-) deprenyl may play a role in the antidepressant effect of this drug in man.

Alkynes↗
PubMed1986

[beta Phenylethylamine: psychopharmacological and clinical aspects].

beta Phenylethylamine (PEA) is an endogenous amine that resembles amphetamine in chemical structure and has been identified in human and other mammalian brains and in many peripheral tissues. Although PEA exists in much smaller amounts than monoamines, the mode of action of PEA as a neuromodulator is of special interest. In this paper the author reviews animal and clinical studies on PEA. The first section deals the methods for the determination of PEA in mammalian brains and human urine. PEA is reliably measured using spectrofluorometric, gas chromatographic-mass spectrometric methods. The second chapter reviews the changes in animal behavior elicited by PEA. The administration of PEA induces stereotypy and increased motor activity in animals. The third part reviews the effect of PEA on dopamine, noradrenaline, serotonin and tyramine metabolism in mammalian brains. The fourth chapter examines recent clinical evidence suggesting a role for PEA in schizophrenia and affective disorders.

Animals↗
PubMed1988

Comparative effects of amphetamine, phenylethylamine and related drugs on dopamine efflux, dopamine uptake and mazindol binding.

We quantified the effects amphetamine (AMPH), phenylethylamine (PEA), tyramine (TYR), octopamine (OCT) and DA, on initial rates of DA uptake (striatal minces), binding of [3H]mazindol to the neuronal uptake (NU) site (striatal membranes) and on DA and dihydroxyphenylacetic acid (DOPAC) efflux (striatal slices). In general, the order of potency for the three paradigms was: AMPH less than DA = TYR = PEA less than OCT. The Km values for uptake were positively correlated with the Ki values for inhibition of mazindol binding (r = 0.91; P less than .01) and with the potencies to induce DA efflux (r = 0.96; P less than .005). Potencies for inhibition of mazindol binding and for eliciting DA efflux also were highly correlated (r = 0.92; P less than .01). Correlations were lost if data for nomifensine (NOM), a NU inhibitor, were included in the analysis. Despite the significant correlations, AMPH, TYR, PEA and OCT Despite the significant correlations, AMPH, TYR, PEA, and OCT were 10 to 20 times more potent in inhibiting NU than in eliciting efflux or inhibiting mazindol binding. Conversely, the potency of NOM to inhibit mazindol binding was 10 and 800 times greater than that required to inhibit NU or to elicit DA release, respectively. NOM inhibited competitively AMPH-induced DA release. These results suggest that: 1) AMPH-like drugs bind to and are likely to be transported by the NU carrier, and 2) inward transport of these agents appears to have multiple effects (e.g., an increase in intracellular Na+ and Cl-) that act cooperatively to increase Vmax and reduce Km for the outward, carrier-mediated DA transport. AMPH, TYR, PEA and OCT had qualitatively similar effects on endogenous DA and [3H]DA release. Monoamine oxidase inhibition potentiated these effects. All these agents released more endogenous DA from control than from reserpine-treated slices. In control slices, TYR and OCT increased DA and DOPAC efflux; whereas AMPH and PEA increased DA and reduced DOPAC efflux, except at high concentrations in which DOPAC efflux also was increased. After reserpine, these agents reduced DOPAC efflux in proportion to the increased DA efflux. In summary, we propose that AMPH-like drugs increase DA efflux from a single cytoplasmic pool maintained by DA synthesis and spontaneous and drug-induced efflux of DA from storage vesicles.(ABSTRACT TRUNCATED AT 400 WORDS)

3,4-Dihydroxyphenylacetic Acid↗