Increase in urinary beta-phenylethylamine preceding the switch from mania to depression: a "rapid cycler".

beta-Phenylethylamine (PEA), an endogenous amphetamine-like substance, is known to increase central catecholamine metabolism and has been hypothesized to have an etiological importance in affective disorders. A case of a "rapid cycler" who showed increased PEA excretion before the switch from mania into depression was reported. In order to evaluate whether the patient's cycle of moods could be prevented by modulating PEA metabolism, carbidopa (peripheral dopa decarboxylase inhibitor) and safrazine (monoamine oxidase inhibitor) were administered during the manic and depressive periods of the patient, respectively. Carbidopa exacerbated the manic symptoms, although it decreased PEA excretion. Safrazine induced the increase of PEA without any beneficial effect on the depressive symptoms. These findings may suggest that PEA plays the role of a biochemical trigger in the switch mechanism of a rapid cycler, especially in the switch from mania to depression.

beta-Phenylethylamine and reinforcement.

beta-Phenylethylamine is an endogenous brain amine which has been characterised as an endogenous amphetamine. The rewarding properties of the structurally similar drug amphetamine in humans and other species indicate a possible role for endogenous beta-phenylethylamine in neural processes underlying reward or reinforcement. Evidence for reinforcing properties of beta-phenylethylamine in the drug self-administration and place preference paradigms is briefly reviewed. The possibility that endogenous beta-phenylethylamine may be involved in reinforcement processes is also considered in relation to studies of intracranial self-stimulation. The contrasting aversive stimulus properties of beta-phenylethylamine and of amphetamine are described.

[Inhibition of gamma-amylase of the rabbit liver by biogenic amines and products of their oxidative deamination]. / Ingibirovanie gamma-amilazy pecheni krolika biogennymi aminami i produktami ikh okislitel'nogo dezaminirovaniia.

Products of oxidative deamination of biogenic amines (aldehydes) exhibited an inhibitory effect on rabbit liver gamma-amylase activity. The aldehydes, formed after serotonin and 2-phenylethylamine oxidation, proved to be most effective in these systems. Dopamine, noradrenaline and tyramine also caused a slight inhibitory action under these conditions. Biogenic amines and corresponding aldehydes participate apparently in regulation of gamma-amylolysis of glycogen in human and animal organisms.

Urinary phenyl acetate: a diagnostic test for depression?

The compound 2-phenylethylamine is an "endogenous amphetamine" which may modulate central adrenergic functions. 2-Phenylethylamine is mainly metabolized by monoamine oxidase to form phenyl acetate (PAA). The 24-hour urinary excretion of PAA was measured in normal healthy volunteers and depressed patients. Patients were diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders, edition 3. In 70 percent of healthy volunteers of both sexes, the excretion of PAA ranged between 70 and 175 milligrams per 24 hours (mean = 141.1 +/- 10.2). Inpatients with major depressive disorder (unipolar type) (N = 31) excreted less PAA (68.7 +/- 7.0 milligrams per 24 hours) and 55 percent of them excreted less than 70 milligrams per 24 hours; there were no significant differences in the PAA excretion between untreated patients (N = 13) and those treated with antidepressants that were not effective (N = 18). The PAA excretion was reduced to a lesser extent in 35 less severely depressed unipolar outpatients (drug-free for 1 week) (86.3 +/- 11.8 milligrams per 24 hours). These results suggest that low PAA urinary excretion may be a reliable state marker for the diagnosis of some forms of unipolar major depressive disorders.

Lithium prevention of amphetamine-induced 'manic' excitement and of reserpine-induced 'depression' in mice: possible role of 2-phenylethylamine.

Repeated treatment of mice with lithium chloride (45 mg/kg, i.p., daily for 8 days) reduced the jumping, fighting, stereotypies, and hyperactivity induced by d-amphetamine (5 mg/kg, i.p.). Lithium also reduced the hypoactivity observed 1--3 h after reserpine (0.75 mg/kg, i.p.). In biochemical studies we found that 8-day treatment with lithium markedly reduced (to 45% of control) the recovery from brain of labelled 2-phenylethylamine (PEA) following i.p. injection of labelled L-phenylalanine, while decreasing recovery from brain of labelled PEA following its i.p. injection of 63% of control. In saline-treated mice, d-amphetamine appeared to increase PEA synthesis and to accelerate its disposition, whereas reserpine enhanced PEA synthesis and reduced disposition; all of these effects were antagonized by lithium pretreatments. Since PEA appears to be one of the most powerful behavioral stimulants among endogenous neuroamines, and because its deaminated metabolites are behavioral depressants, such antagonism of brain PEA metabolism may significantly contribute to the prophylactic action of lithium against both manic and depressive behavior.

Phenylethanolamine: a new putative neurotransmitter in Aplysia.

Phenylethanolamine is present in the Aplysia nervous system in concentrations similar to that of octopamine. These are receptors that are very specific for phenylethanolamine, which on different neurons mediate sodium, chlorine, or potassium conductance increase responses. These observations indicate that phenylethanolamine may act as a neurotransmitter in Aplysia.