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PubMed1984

Depression during methadone withdrawal: no role for beta-phenylethylamine.

An atypical depression, resembling beta-phenylethylamine (PEA) deficiency states, frequently complicates methadone withdrawal. We undertook a study of 24-h urinary free PEA excretion in steady-dosed and withdrawing methadone patients, hypothesizing that abstinent patients would excrete less PEA than controls and that methadone would show a dose-dependent effect on PEA turnover. As hepatic dysfunction, frequent in methadone patients, might affect PEA turnover, we also evaluated liver chemistries, [13C]aminopyrine excretion, 2-hydroxylation of estradiol, and 'blind', global severity ratings in each subject. PEA excretion did not significantly differ between eight fully detoxified methadone patients (median 4.76 micrograms/24 h) and seven normal controls (median 5.80 micrograms/24 h). Moreover, PEA excretion bore no relation to methadone dosage among 24 steady-dosed subjects. PEA excretion in seven withdrawing subjects each receiving 4-8 different doses of methadone similarly showed no relation to dose. Despite significant liver disease, several measures of impairment did not correlate with PEA excretion. These findings argue against a role for PEA deficiency in withdrawal depression.

2-Hydroxyphenethylamine↗

PubMed1986

A review of the effects of repeated administration of selected phenylethylamines.

Several phenylethylamines are under consideration for international control. The effects of repeated administration of these compounds, including tolerance, physical dependence and central nervous system (CNS) toxicity, are reviewed here. The compounds can be divided into two major chemical groups: those with substituents on the ethylamine portion of the molecule and those with substituents on the phenyl ring. Although the effects of repeated administration have not been directly determined for most of the compounds, certain representative compounds of each chemical group have been examined in some detail. Prominent among the effects of repeated administration are CNS toxicity and tolerance development. Physical dependence has not been reported for any of these compounds. Future research with these compounds should emphasize the investigation of the CNS toxicity and the functional consequences of such effects for the organism.

3,4-Methylenedioxyamphetamine↗

PubMed1992

Determination of urinary beta-phenylethylamine as its N-benzenesulphonamide derivative by gas chromatography with flame photometric detection.

A selective and sensitive method for the determination of urinary beta-phenylethylamine (PEA) by gas chromatography (GC) has been developed. After extraction of the urine sample with n-pentane, PEA was converted into its N-benzenesulphonamide derivative and then determined by GC with flame photometric detection using a DB-1301 capillary column. By using this method, nanogram amounts of PEA in urine could be accurately and precisely determined without any influence from coexisting substances. Analytical results for the determination of PEA in urine samples from normal subjects are presented.

Chromatography, Gas↗

PubMed1996

Sensitive high-performance liquid chromatographic method for the determination of 2-phenylethylamine in human urine.

A new sensitive high-performance liquid chromatographic (HPLC) method with fluorescence detection was developed for the determination of 2-phenylethylamine (PEA) in human urine. The analytical procedure involved a simple extraction of the analyte from urine, followed by precolumn derivatisation of the sample with o-phthalaldehyde. The HPLC separation was performed under isocratic conditions using an Erbasil S C18 (250 x 4.0 mm I.D., particle size 3 microns) reversed-phase column. The limit of quantitation was 0.5 ng of PEA/ml of urine. The method showed good linearity, accuracy and precision data in the concentration range 0.5-200 ng/ml of urine. The method was successfully applied to the determination of PEA urinary excretion in Parkinsonian patients after oral administration of the monoamine oxidase B (MAO-B) inhibitor, selegiline.

Aged↗

PubMed1995

Amides of piperidine, morpholine and piperazine substituted 1-phenylethylamines: inhibitors of acylCoA:cholesterol acyltransferase (ACAT) activity in vitro and in vivo.

Amides of some substituted 1,2-diarylethylamines have been shown to exhibit potent acylCoA:cholesterol acyltransferase (ACAT, EC 2.3.1.26) inhibitory activity in vitro in microsomal ACAT assays but show poor in vivo activity in a cholesterol-fed hamster model. In an effort to design ACAT inhibitors that are potent in both our in vitro and in vivo assays a series of amides of piperidine, morpholine and piperazine substituted 1-phenylethylamines were synthesized. Compounds of this series were found to be very potent inhibitors of ACAT in a microsomal ACAT assay and also exhibited potent activity in a cholesterol-fed hamster model.

Amides↗

PubMed2004

Behavior and characteristics of the o-phthaldialdehyde derivatives of n-C6-C8 amines and phenylethylamines with four additive SH-containing reagents.

The stability and characteristics of the C6-C8 n-aliphatic and phenylethylamines have been investigated as their o-phthaldialdehyde (OPA)/3-mercaptopropionic acid, OPA/N-acetyl-L-cysteine, OPA/2-mercaptoethanol and OPA/ethanethiol derivatives. Stoichiometric studies have been followed by photodiode array and fluorescence detection, simultaneously, while the composition of derivatives was confirmed by on line HPLC-electrospray ionization (ESI)-MS measurements. All four amines having in their original structure the NH2-CH2- moiety in accordance with the C1-C4 aliphatic, mono and diamines and amino acids of the same structure--furnished more than one OPA derivative: their initially formed isoindoles transform to further ones. Depending on the composition of the OPA reagents and on the pH of derivatizations different type of transformed species have been identified, in various proportions. Applying the OPA/SH additive reagent in the molar ratio of 1/3, favors the formation of one additional OPA molecule-containing isoindole, while using the OPA/SH additive (1/50) reagent resulted in the formation of one additional SH additive-containing species, identified and measured at the first time by HPLC. Transformation rate and stability of derivatives proved to be associated with the composition of the OPA reagent, with the type of the SH additive, with the pH of derivatizations, and, in selected cases also with the chain length of the amine. Results of stoichiometric and mechanism studies have been utilized to define optimum analytical conditions.

Amines↗

PubMed2005

Enantiomeric separation of 1-phenylethylamine and 1-cyclohexylethylamine in capillary electrophoresis with contactless conductivity detection.

Contactless conductivity detection was employed for the detection of the enantiomers of 1-phenylethylamine and 1-cyclohexylethylamine which were separated in capillary electrophoresis with unprecedented high resolutions R(s) of 2.3 and 3.3, respectively, by using a combination of dimethyl-beta-cyclodextrin and the chiral crown ether 18C6H4 as chiral selectors in a citric acid buffer of pH 2.4. The conductivity measurement enabled the direct detection, i.e. without having to derivatize or resort to indirect methods, of all species including the non-UV-absorbing enantiomers of cyclohexylamine. Detection limits of 0.5 microM were achieved and the determination of enantiomeric ratios of up to 99:1 was found possible.

Electric Conductivity↗

PubMed2005

2-Phenylethylamine in combination with l-deprenyl lowers the striatal level of dopamine and prolongs the duration of the stereotypy in mice.

2-Phenylethylamine (PEA)-induced stereotypy in rodents is suggested to model psychotic symptoms of schizophrenia. It is reported that PEA induces dopamine release in the striatum in vivo and in vitro. The present study analyzed the PEA-induced stereotypy and possible associated brain dopamine metabolism in mice. Using male ICR mice treated with a combination of PEA (100 mg/kg, i.p.) and increasing doses of l-deprenyl (0-10 mg/kg, s.c.), we examined (1) the behavioral profile of stereotypy (rating the scores), and (2) the tissue levels of dopamine and its metabolites by high-performance liquid chromatography. The stereotypic scores reached a plateau level at 10 min which lasted until 30 min after a single administration of 100 mg/kg PEA. The stereotyped behavior completely disappeared 45 min after PEA administration. Pretreatment with l-deprenyl (0.1, 1, and 10 mg/kg, s.c.) dose-dependently prolonged the duration of PEA-induced stereotypy. Notably, pretreatment with l-deprenyl dose-dependently increased the continuous sniffing. Treatment with PEA in combination of l-deprenyl (1 and 10 mg/kg) significantly reduced the level of dopamine in the region of the striatum and nucleus accumbens, compared with control animals. These results suggest that PEA in combination with l-deprenyl prolonged the duration of the stereotypy (particularly, continuous sniffing) while reducing the striatal level of dopamine.

Animals↗

PubMed2004

Pharmacological studies with endogenous enhancer substances: beta-phenylethylamine, tryptamine, and their synthetic derivatives.

The discovery of enhancer regulation in the mesencephalon and the concept that it plays a key role in the operation of innate and acquired drives [Neurochem. Res. 28 (2003) 1187] sets the trace amines (TAs) in their true physiological perspective. The regulation is defined as the existence of enhancer-sensitive neurons in the brain capable of working in a split-second on a high activity level due to endogenous enhancer substances. For the time being, only beta-phenylethylamine (PEA) and tryptamine are the experimentally analyzed examples. (-)-Deprenyl (selegiline), widely used in Parkinson's disease and Alzheimer's disease today, and known as the first selective monoamine oxidase (MAO) type-B inhibitor for decades, was identified as a PEA-derived synthetic mesencephalic enhancer substance. An important and convincing confirmation of the enhancer concept was the recent development of a highly specific and potent tryptamine-derived synthetic mesencephalic enhancer substance, (-)-1-(benzofuran-2-yl)-2-propylaminopentane [(-)-BPAP]. This substance, which is specific and hundreds of times more potent than selegiline, is now the best experimental tool to study the enhancer regulation in the mesencephalon and a promising candidate to significantly surpass the therapeutic efficiency of selegiline in depression, Parkinson's disease, and Alzheimer's disease.

Animals↗

PubMed2000

Effects of beta-phenylethylamine on the hypothalamo-pituitary-adrenal axis in the male rat.

beta-Phenylethylamine (PEA) is a trace neuroactive amine implicated in the regulation of the hypothalamic-pituitary-adrenal (HPA) response to stress. To test this hypothesis, effects of subchronic levels of PEA (50 mg/kg/day treatment for 10 days) on the corticotroph function were studied. PEA treatment induces: (i) a significant increase of corticotrophin releasing hormone (CRH) immunoreactivity in the median eminence (ME), as measured by semi-quantitative immunofluorescence labeling techniques, (ii) a significant increase in CRH mRNA levels in paraventricular nuclei, as detected by in situ hybridization, and (iii) an increase in plasma adreno-corticotrophin hormone (ACTH) and corticosterone levels in responses to stress. PEA treatment has no effect on the number of binding sites and on the dissociation constant of the glucocorticoid receptors in any structure studied. Results of the dexamethasone suppression test were similar in PEA- and saline-treated rats. Taken together, these results suggest that PEA treatment stimulated the HPA axis activity levels directly via the CRH hypothalamic neurons, without altering the negative feed back control exerted by the glucocorticoids.

Adrenocorticotropic Hormone↗

PubMed2003

Behavioral characterization of 2-O-desmethyl and 5-O-desmethyl metabolites of the phenylethylamine hallucinogen DOM.

The present investigation was undertaken to test the hypothesis that known metabolites of the phenylethylamine hallucinogen 1-(2,5-dimethoxy-4-methylphenyl)-2-aminopropane (DOM) are pharmacologically active. This hypothesis was tested by evaluating the ability of racemic DOM metabolites 2-O-desmethyl DOM (2-DM-DOM) and 5-O-desmethyl DOM (5-DM-DOM) to substitute for the stimulus properties of (+)lysergic acid diethylamide (LSD). The data indicate that both metabolites are active in LSD-trained subjects and are significantly inhibited by the selective 5-HT(2A) receptor antagonist M100907. Full generalization of LSD to both 2-DM-DOM and 5-DM-DOM occurred, and 5-DM-DOM was slightly more potent than 2-DM-DOM. Similarly, 5-DM-DOM had a slightly higher affinity than 2-DM-DOM for both 5-HT(2A) and 5-HT(2C) receptors. Additionally, it was of interest to determine if the formation of active metabolite(s) resulted in a temporal delay associated with maximal stimulus effects of DOM. We postulated that if metabolite formation resulted in the aforementioned delay, direct administration of the metabolites might result in maximally stable stimulus effects at an earlier pretreatment time. This hypothesis was tested by evaluating (1) the time point at which DOM produces the greatest degree of LSD-appropriate responding, (2) the involvement of 5-HT(2A) receptor in the stimulus effects of DOM at various pretreatment times by administration of M100907 and (3) the ability of 2-DM-DOM and 5-DM-DOM to substitute for the stimulus properties of LSD using either 15- or 75-min pretreatment time. The data indicate that (a) the DOM stimulus produces the greatest degree of LSD-appropriate responding at the 75-min time point in comparison with earlier pretreatment times and (b) the stimulus effects of DOM are differentially antagonized by M100907 and this effect is a function of DOM pretreatment time prior to testing. Both 2-DM-DOM and 5-DM-DOM were found to be most active, at all doses tested, using a 75-min versus a 15-min pretreatment time. The present data do not permit unequivocal acceptance or rejection of the hypothesis that active metabolites of (-)-DOM provide a full explanation of the observed discrepancy between brain levels of (-)-DOM and maximal stimulus effects.

DOM 2,5-Dimethoxy-4-Methylamphetamine↗

PubMed1997

Does phenylethylamine have a role in schizophrenia?: LSD and PCP up-regulate aromatic L-amino acid decarboxylase mRNA levels.

Aromatic L-amino acid decarboxylase (AADC) is rate limiting in the production of 2-phenylethylamine (2PE). AADC activity and 2PE serum concentrations have been found to be increased in schizophrenic patients. Both antipsychotic and psychotogenic drugs, including amphetamine, affect the activity and encoding mRNA levels of AADC. Amphetamine is an analogue of 2PE and has a similar physiological effect. We have looked at the effects of chronic (32 day) treatment of rats with LSD (0.12 microg/kg/day) and phencyclidine (PCP; 10 mg/kg/day) on AADC mRNA levels. Both drugs up-regulated AADC mRNA levels in striatum, nucleus accumbens, hippocampus and cerebellum by between 50% and 150%. A splicing variant of AADC, present in human brain, which lacks the 3rd exon does not appear to be present in rat brain. These results are consistent with the hypothesis that over activity of AADC leading to increased production of 2PE is involved in endogenous psychosis such as schizophrenia.

Alternative Splicing↗

PubMed1982

An observational analysis of the behavioural effects of beta-phenylethylamine in isolated and grouped mice.

1. Male Swiss mice were treated systemically with beta-phenylethylamine (PEA, 25-150 mg/kg), and observed in isolation or in groups of five. The effects of PEA were scored on 13 separate components of behaviour which were produced or increased by the drug. 2. PEA at a dose of 25 mg/kg depressed activity and caused sedation, but at 50 mg/kg produced a brief stimulation of activity. At higher dose levels (75-150 mg/kg) the compound induced a biphasic stimulation of activity which was associated with the development of two distinct groups of stereotyped activities. 3. Group testing significantly antagonized early phase stereotypy (forepaw padding, headweaving, compulsive grooming) but had no effect on, or potentiated, late phase stereotypy (rearing, licking). In addition grouped mice were more active and hyperreactive than isolated mice. 4. The results are briefly discussed in the light of the possibility of a catecholamine/indoleamine interaction in the control of the hyperactivity syndrome induced by PEA in the mouse.

Animals↗

PubMed1998

Alpha 1-adrenergic and 5-HT2-serotonergic effects of some beta-alkoxy-beta-phenylethylamines on isolated rat thoracic aorta.

1. Ten racemic beta-alkoxy-beta-phenylethylamines were found to elicit concentration-dependent contraction of the isolated rat thoracic aorta with apparent pD2 values in the 4.56-6.76 range. With one exception, which produces the same maximal contraction (Emax) as serotonin (5-HT), the Emax values attained with these compounds are lower than those produced by either 5-HT or norepinephrine (NE). 2. Pretreatment with either prazosin or ketanserin (10(-8) M) leads in most cases to decreased Emax values and slopes in the dose-response curves. Apparent serotonergic (pD2S) and adrenergic (pD2A) pD2 values going from 4.22 to 6.08 (pD2S) and from 3.87 to 5.27 (pD2A) were calculated from results obtained in the presence of prazosin or ketanserin, respectively. 3. In the 10(-7)-10(-5) M range, and in contrast with the results obtained with the previous compounds, BON [(+/-)-2-(2,5-dimethoxy-4-nitrophenyl)-2-methoxy-ethylamine] behaves as an antagonist to both 5-HT and NE (apparent pA2 = 7.08 and 7.45, respectively) in this preparation.

Adrenergic alpha-1 Receptor Agonists↗

PubMed1979

Urinary phenylethylamine excretion: gas chromatographic assay with electron-capture detection of the pentafluorobenzoyl derivative.

Phenylethylamine was extracted into n-hexane from alkaline urine saturated with sodium chloride, and back-extracted into dilute acid. The extract was freeze-dried and the residue converted to a pentafluorobenzoyl derivative for analysis by gas chromatography on a column of OV-225 with electron-capture detection. Quantification was achieved by adding an internal standard of tolylethylamine to each sample prior to extraction. Output values in normal subjects and in some patients with phenylketonuria and hyperphenylalaninaemia were in agreement with those in some other recent reports.

Adult↗

PubMed1986

Electron-capture gas chromatographic analysis of beta-phenylethylamine in tissues and body fluids using pentafluorobenzenesulfonyl chloride for derivatization.

A gas chromatographic procedure is described for the analysis of beta-phenylethylamine (PEA) in tissues and body fluids. The method involves the use of pentafluorobenzenesulfonyl chloride for extraction and derivatization of PEA. This is followed by separation and analysis of the derivatized amine on a gas chromatograph equipped with a fused-silica capillary column and an electron-capture detector. The procedure is rapid, provides a stable and sensitive derivative, and has been applied to analysis of PEA in brain, heart, kidney, liver, lung, spleen and blood from the rat and urine from human subjects.

Animals↗

PubMed2001

Alpha-phenylethylamine in illegally produced amphetamine.

The possibility of simultaneous synthesis of alpha-phenylethylamine and amphetamine from mixture of acetophenone and benzylmethylketone was studied. The structures of specific impurities were predicted and these compounds were synthesized and finally found in reaction mixtures, as well as in the final product. The data collected by gas chromatography, proton and carbon magnetic resonance, Fourier transform infrared spectrometry and mass spectrometry are presented.

Amphetamines↗

PubMed2002

Rat striatal monoamine oxidase-B inhibition by l-deprenyl and rasagiline: its relationship to 2-phenylethylamine-induced stereotypy and Parkinson's disease.

Rats were injected intraperitoneally with varying doses of l-deprenyl (selegiline) followed 2h later by 30 mg kg(-1) 2-phenylethylamine (PEA), administered in the same way, and the stereotypic behavioural response elicited was assessed. l-Deprenyl alone at doses of up to 5 mg kg(-1) caused no significant behavioural response. Administration of PEA without prior l-deprenyl treatment resulted in only a modest increase in stereotypic behaviour and this was not significantly enhanced by the prior administration 1 mg kg(-1) l-deprenyl. When the administered dose of l-deprenyl was increased to 2.5 or 5 mgkg(-1), however, the stereotypic behavioural response to PEA was greatly potentiated and in the latter case persisted for 60 min. A dose of 2.5 mg kg(-1) l-deprenyl and 1 mg kg(-1) rasagiline was shown to result in over 90% inhibition of the monoamine oxidase (MAO)-B from rat liver and striatum, whereas the inhibition of MAO-A was about 60 and 40% in liver and striatum, respectively. The recovery of MAO-B activity in rat striatum and liver following a single i.p. injection of 5 mg kg(-1) l-deprenyl gave first-order rate constants of 1.80 and 7.15 h(-1), respectively, which corresponded to half-lives of 9.23 and 2.33 days. Similar results were obtained with rasagiline. The corresponding indices of stereotypic response to PEA (30 mg kg(-1); i.p.) during recovery from the single dose of l-deprenyl were initially high, but had started to decline by the third day after l-deprenyl treatment and was not significant after day 4. At that time, less than 20% of the striatal monoamine oxidase-B activity had been regained, whereas the recovery of the liver enzyme was about 65%. These data are discussed in terms of the suggested involvement of PEA potentiation in the anti-parkinsonian actions of l-deprenyl and rasagiline and the duration of the 'wash-out' period used in studies on the effects of l-deprenyl on patients with Parkinson's disease. The longer duration of the recovery of brain monoamine oxidase B after its selective inhibition and the corresponding behavioural responses of the animals to PEA at same time points, indicate that PEA may have a major pharmacological role in the mechanism of the antiParkinson action of l-deprenyl and rasagiline. Brain monoamine oxidase B inhibition has previously been shown to significantly increases brain PEA and which is capable of releasing dopamine endogenously or that formed from L-dopa.

Animals↗