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At least 217 records · Page 12Linked to original sources

PubMed1982

Fluctuating high urinary phenylethylamine excretion rates in some bipolar affective disorder patients.

Five women with primary major bipolar affective disorders had variable and at times very high urinary phenylethylamine (PEA) excretion rates. The clinical picture of these patients was characterized by periodic bizarre behaviors and short psychotic episodes. These patients were generally nonresponsive to the usual treatment modalities, and their symptoms were exacerbated by nonspecific monoamine oxidase inhibitors which further increased PEA excretion rates.

Adolescent↗

PubMed1984

Phenylethylamine excretion in depression.

Urinary phenylethylamine (PEA) excretion was evaluated in two populations of depressed hospitalized patients. Seven of 53 patients had PEA values exceeding three times the highest value found in 16 normal controls. The patients with high PEA excretion were all females. They were not, however, otherwise clinically distinguishable from depressed patients with low PEA. In a subsample of 31 patients and 10 controls, PEA excretion was not correlated with phenylacetic acid (PAA) excretion. These results suggest that depression is not associated with a generalized PEA deficit and that PAA reductions, previously reported in a depressed patient population, may not reflect a PEA abnormality.

Adolescent↗

PubMed1990

Urinary amines in Tourette's syndrome patients with and without phenylethylamine abnormality.

Previous data indicated a subgroup of Tourette's syndrome patients with a beta-phenylethylamine (PEA) level that was lower than all subjects in a control group matched for age and education. The current study compared the subgroups of Tourette's syndrome patients (n = 28) from the previous study with 20 control subjects in regard to other amines and metabolites. Patients with low levels of PEA were also found to have lower levels of 3-methoxy-4-hydroxy-phenylglycol, normetanephrine, serotonin, m-tyramine, and p-tyramine. There was also some evidence of dopaminergic abnormalities in the low-PEA subgroup. These data provide suggest a role of PEA in the pathophysiology of some patients with Tourette's syndrome. This effect may be mediated through other neurotransmitter systems.

Adolescent↗

PubMed1987

Presynaptic alpha 2-adrenoceptors exclusively sensitive to agonists of phenylethylamine structure on the sympathetic nerves of the human gall bladder artery.

The influence of alpha 2-adrenoceptor agonists and antagonists on the release of noradrenaline was studied in human gall bladder (cystic) artery preparations, in which transmitter stores were labelled with [3H]noradrenaline. The preparations were stimulated at 2 Hz for 3 min (360 shocks each of 1 ms duration two times (S1 and S2)). Both the L-noradrenaline and alpha-methylnoradrenaline (10(-6) M) significantly reduced (S2/S1 = 0.27 +/- 0.05; 0.43 +/- 0.04, respectively), whilst clonidine, xylazine and guanfacine at 10(-6) M failed to affect the stimulation evoked release of [3H]noradrenaline. Yohimbine (10(-6) M), CH-38083, which is a new, selective alpha 2-adrenoceptor antagonist (10(-7) M) and prazosin (10(-6) M) enhanced the evoked release of radioactivity, where S2/S1 were 2.50 +/- 0.19; 2.99 +/- 0.32; 1.48 +/- 0.05, respectively. Administering the alpha 2-antagonists and prazosin together, we were unable to demonstrate an additive effect. Yohimbine and CH-38083 prevented, while prazosin reduced, the inhibitory effects of L-noradrenaline or alpha-methylnoradrenaline on the release of radioactivity. Our results suggest that one type of presynaptic alpha 2-adrenoceptor modulates the release of noradrenaline evoked by electrical stimulation of the human cystic artery. This receptor is sensitive to alpha 2-adrenoceptor agonists which have a phenylethylamine structure, but is insensitive to imidazolines and guanfacine.

Adrenergic Fibers↗

PubMed1983

The effects of beta-phenylethylamine on tyramine and dopamine metabolism.

The administration of deuterated beta-phenylethylamine to mice causes increased concentrations of deuterated para-hydroxyphenylacetic acid and meta-hydroxyphenylacetic acid within the caudate nuclei two hours after injection. Deuterated m-HPAA concentrations remain elevated at 4 hours. This suggests that high concentrations of PE stimulate synthesis of the tyramines and thus of their deaminated metabolites. Deuterated PE causes rapid increases in the concentrations of endogenous nondeuterated p-HPAA and m-HPAA. p-HPAA concentrations remain elevated two hours after PE administration. Thus PE mobilizes the tyramines and produces elevated concentrations of their deaminated products. PE injected into rats initially increases 3-MT concentrations in the caudate nuclei. DOPAC concentrations are elevated five minutes later followed by elevated HVA concentrations. DA synthesis is also stimulated. The PE dependent increase in DA release into the synaptic cleft (3-MT increases) and DA synthesis also appear to lead to increased intraneuronal DA metabolism (DOPAC increases).

3,4-Dihydroxyphenylacetic Acid↗

PubMed1983

Pharmacology of beta-phenylethylamine-induced seizures in mice.

The endogenous trace amine beta-phenylethylamine (PE) produced tonic-clonic seizures in male Swiss mice when administered in doses of 125-200 mg/kg. The number of mice exhibiting PE-induced seizures, the latency to onset of first seizure and the latency to loss of the righting reflex were dose dependent. Pretreatment with the benzodiazepines diazepam, chlordiazepoxide, midazolam and clonazepam significantly reduced the incidence of PE-induced seizures. Similarly, increasing brain gamma-aminobutyric acid (GABA) levels by injection of the GABA-transaminase inhibitors aminooxyacetic acid or gabaculine afforded significant protection against PEA's convulsant effects. The data suggest that PE when administered at high doses may interfere either directly or indirectly with GABAergic neurotransmission in the central nervous system. In addition, since PE induces an epileptiform spiking pattern and produces seizures in rodents it appears possible that the amine may play a role in some forms of human epilepsy.

Animals↗

PubMed1983

Release of monoamines from striatal slices by phenelzine and beta-phenylethylamine.

Slices of striatum obtained from control rats were incubated with 3H-serotonin (3H-5HT) or 14C-dopamine (14C-DA) in the presence of pargyline; then, they were subjected to a rapid transfer technique during which they were washed either with a normal Krebs buffer or one containing known quantities of phenelzine (PEH) or beta-phenylethylamine (PE). Both PEH and PE were able to stimulate releases of 3H-5HT and 14C-DA that were greater than control. More 14C-DA than 3H-5HT was released by both compounds. Much lower concentrations of PE than of PEH were required to stimulate monoamine release. Other rats were injected intraperitoneally with behaviourally effective doses of either PEH or PE and were killed at various times. The concentrations of PEH or of PE in the striata of these animals were very high 15 min after I.P. injection, but declined rapidly thereafter. These results may be interpreted to suggest that after I.P. injection, sufficient levels of PEH and PE were attained in the rat striatum to stimulate release of endogenous 5HT and DA.

Animals↗

PubMed1984

Brain levels of 5-hydroxytryptamine, tryptamine and 2-phenylethylamine in the rat after administration of N-cyanoethyltranylcypromine.

Brain levels of 5-hydroxytryptamine (5-HT), tryptamine (T), 2-phenylethylamine (PEA) and monoamine oxidase activity at 5, 15, 30, 60, 120 and 240 min were determined in male Sprague-Dawley rats after intraperitoneal injection of the "pro-drug" N-2-cyanoethyltranylcypromine (CE-TCP, dose 0.1 mMole/kg). Analyses of 5-HT, T and PEA were performed on an electron-capture gas chromatograph with a capillary column. Activity of MAO-A and MAO-B was measured using a radiochemical method. Results indicate substantial inhibition of MAO in rat brain after intraperitoneal administration of CE-TCP, leading to elevated levels of 5-HT, T and PEA as early as 5 min after drug administration. Increases in brain levels of the trace amines T and PEA were much greater (approximately 40 and 100 times control levels, respectively) than with 5-HT (approximately 1.8 times control level) 240 min after administration of CE-TCP.

Animals↗

PubMed1992

Beta-phenylethylamine and noradrenergic function in depression.

1. The relationship between plasma levels of beta-phenylethylamine (PEA) and 3-methoxy-4-hydroxyphenylglycol (MHPG) was investigated in depressive patients. 2. The mean PEA level in plasma in healthy subjects was 1.19 ng/ml (N = 32). No clearly age-related difference was found. The plasma levels of PEA were measured in major depression, but no significant difference was found between healthy and depressive subjects. 3. Plasma levels of MHPG correlated positively with age in healthy subjects (N = 22, R = 0.71, p less than 0.01). There was no significant difference in MHPG levels between healthy subjects and depressive patients. 4. There was no significant correlation between PEA and MHPG levels in healthy subjects; however, in depressive patients, there was a significant negative correlation between plasma PEA levels and plasma MHPG levels (N = 14, R = -0.73, p less than 0.05). These results suggested that PEA may regulate noradrenergic function in depression.

Depressive Disorder↗

PubMed1994

Phenylethylamine and schizophrenia.

1. The evidence that phenylethylamine (PEA) plays a role in the etiology of schizophrenia is reviewed. 2. PEA shares structural and physiological similarities with the amphetamines, the administration of which can induce a schizophrenia-like psychosis. 3. While there are a number of reports of high urinary PEA excretion in schizophrenic patients, the measurement of PEA in other body fluids and the measurement of phenylacetic acid (the major metabolite of PEA) has resulted in inconsistent findings. 4. The use of neuroleptic medication is a major confounding variable in most of the clinical studies. If PEA does have a role in the etiology of schizophrenia, the mechanism may involve PEAs ability to amplify dopamine responses.

Antipsychotic Agents↗

PubMed1988

The potentiation of cortical neurone responses to noradrenaline by beta-phenylethylamine: effects of lesions of the locus coeruleus.

beta-Phenylethylamine (PE) potentiates single cortical neurone responses to noradrenaline (NA). The hypothesis that this is due to an action on the noradrenergic presynaptic terminal was tested. Extracellular recordings of the responses of single cortical neurones to iontophoretically applied NA and PE were made in rats with unilateral electrolytic lesions of the locus coeruleus. Ipsilateral lesions blocked responses to PE but did not affect the ability of PE to enhance responses to NA. Contralateral lesions had no effect on either the responses to PE or the enhancement of responses to NA. It is concluded that the PE-induced potentiation of responses to NA is not due to a presynaptic action of PE.

Animals↗

PubMed1983

Phenylethylamine in neuropsychiatric disorders.

Phenylethylamine is an endogenous neuroamine conceptualized as the body's natural amphetamine. PEA has been suggested to play a role in the etiology of several neuropsychiatric disorders. Increased PEA turnover in phenylketonuria contributes to the pathophysiology of this condition. Depressed and chronic paranoid schizophrenic patients show decreased and increased PEA urinary excretion, respectively. Parkinsonian patients show decreased urinary PEA excretion. In animals, drugs that relieve or produce depression and parkinson result in increased or decreased brain PEA levels, respectively. PEA has been postulated to play a role in the etiology of migraine headache and aggression.

Affective Disorders, Psychotic↗

PubMed1985

Examination of the bronchoconstrictor response of guinea-pig isolated lung to beta-phenylethylamine.

beta-Phenylethylamine (PEA) produced a contraction of the guinea-pig isolated lung parenchymal strip and bronchoconstriction of perfused lungs. Reserpine pretreatment had little effect on these responses indicating a substantial direct effect. Phentolamine (10(-6) and 10(-5) M) had minimal effect on PEA in the lung strip compared with that on noradrenaline, eliminating involvement of alpha-adrenoceptors. PEA was unaffected by atropine (10(-7)M) or a mepyramine (10(-7)M); metiamide (10(-4)M) mixture. The contraction was not therefore mediated via muscarinic or histaminergic receptors. 5-HT and dopamine receptors were also discounted. Possible stimulation of a phenylethylaminergic receptor and its relevance to bronchial asthma is discussed.

Animals↗

PubMed1989

The most desirable conformation of phenylethylamine (PEA) moiety stimulating noradrenergic neurons: effects of PEA, methamphetamine, phenelzine, methylphenidate, nomifensine and mazindol on rat spinal reflexes.

1. The effects of phenylethylamine (PEA) and PEA-related substances on the rat spinal monosynaptic reflex (MSR) were examined. According to the flexibility of the PEA moiety in the molecule, these drugs were classified into three groups, i.e. non-rigid, rigid and semi-rigid groups. 2. PEA, methamphetamine and phenelzine (non-rigid group) showed opposite effects on the MSR, an increase at low doses and a decrease at high doses. The former effect was antagonized by pretreatment with the alpha 1-blocker, prazosin. 3. Nomifensine and mazindol (rigid group), which share the similar spatial relationships between the aromatic moiety and nitrogen, increased the MSR, and this effect was blocked by prazosin. 4. In the semi-rigid group the same result was obtained for methylphenidate but not for 1-methyl-2-benzylpiperidine, which might have difficulty in having the similar conformation of PEA moiety as methylphenidate because of its methyl group. 5. From these results, it appears that the effects of PEA and amphetamines on the MSR are determined by the spatial relationships between the amino group and the aromatic moiety and that the enhancement of the MSR might be induced through alpha 1-adrenergic transmission.

Animals↗

PubMed1994

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

1. 2C-H [2-(2,5-dimethoxyphenyl)ethylamine] (pD2 = 6.74), TMPEA [2,(2,4,5-trimethoxyphenyl)ethylamine] (pD2 = 5.83), 2C-D [2-(2,5-dimethoxy-4-methylphenyl)ethylamine] (pD2 = 5.06), homoveratrylamine [DMPEA, 2-(4,5-dimethoxyphenyl)ethylamine] (pD2 = 4.46) and homopiperonylamine [MDPEA, 2-(3,4-methylenedioxyphenyl)ethylamine] (pD2 = 4.19), elicit concentration-dependent contraction of the isolated rat thoracic aorta. 2. At 9.9 x 10(-6) M, 2C-N [2-(2,5-dimethoxy-4-nitrophenyl)ethylamine] behaves as a competitive antagonist to serotonin in this preparation. 3. Considering previous results with the structurally related 2C-B [2-(4-bromo-2,5-dimethoxyphenyl)ethylamine], weak or partial agonistic activity or antagonism of aortic contraction appears to be related to psychedelic properties reported in humans for phenylethylamines.

Animals↗

PubMed1984

The behavioural effects of phenelzine and phenylethylamine may be due to amine release.

Intraperitoneal administration of phenelzine (PLZ) or of beta-phenylethylamine (PE) quickly leads to short periods of behavioural activation, which are primarily dopaminergic and serotonergic in nature, respectively. In order to determine whether these behavioural effects are due to PLZ- or PE-induced displacement of dopamine (DA) or serotonin (5HT), the ability of these compounds to stimulate release of radiolabelled DA and 5HT from slices of rat striatum was assessed. Additionally, at various times following IP administration of behaviourally active doses of PLZ or PE to rats, the striatal levels of the drugs were measured. Both PLZ and PE were able to stimulate a greater release of radiolabelled DA than of 5HT. Lower concentrations of PE (0.8, 8.0 microM) than of PLZ (100 microM, 1 mM) stimulated release. The striatal levels (approximately 200 microM) of PLZ, as well as of PE, attained at times corresponding to behavioural activation seemed sufficient to cause release of both DA and 5HT. It was concluded, therefore, that the mode of action of these compounds may involve displacement, or release, of these biogenic amines, though it is not clear how such release ultimately leads to the behaviours observed.

Animals↗

PubMed1988

beta-Phenylethylamine enhances single cortical neurone responses to noradrenaline in the rat.

The firing rates of single neurones in the rat cerebral cortex were recorded using multibarrel glass microelectrodes, and the response to drugs applied by microiontophoresis was investigated. A greater number of cells responded to noradrenaline (NA) (30-66 nA) than to beta-phenylethylamine (PE) (30-100 nA). When responses were obtained to both, 90% of the neurones gave the same response to NA and PE. Applications of PE with small currents (0-12 nA) caused an increase in the response to NA without affecting the baseline firing rate or the response to acetylcholine, glutamate, GABA or 5-hydroxytryptamine. An increase was seen in both excitatory and inhibitory responses to NA. The enhancement lasted up to 39 minutes after the end of the PE application. Applications of NA with small currents (0-3 nA) failed to alter responses to NA. Possible mechanisms of the effect of PE on response to NA are discussed. These results provide further evidence for the hypothesis that trace amines can modulate catecholamine neurotransmission.

Animals↗

PubMed1976

Metabolic disposition of 2-phenylethylamine and the role of depression in methadone-dependent and detoxified patients.

We have now postulated that differences in the innate capacity of individuals to synthesize, store and utilize biogenic amines may provide the biological basis for human abuse of narcotic and other drugs, and that these drugs are used in an apparent unconscious effort to self-medicate against an inherent affective disorder. In this communication, we attempted a preliminary characterization of the narcotics withdrawal syndrome on biochemical and clinical parameters. Abstinence was found to be characterized by low urinary excretion of 2-phenylethylamine and depression. An indication for use of tricyclic drugs has been discussed.

Adult↗