Abstract
2-Phenylethylamine (PEA), a compound with stimulant properties when administered to animals, occurs in minute quantities in the normal mammalian brain (Durden et al. 1973). The turnover of this amine is high (Durden and Philips, 1980) and there is no evidence for storage, uptake or impulse-mediated release as yet. PEA, like other trace amines, has been regarded mainly as a metabolic accident in the past (see Boulton, 1984). However, a number of clinical studies with its precursor amino acid, phenylalanine, as well as investigations of its CSF concentrations or the urinary excretion of PEA or its metabolite phenylacetic acid in psychiatric patients seemed to indicate a possible role of the amine in depression, schizophrenia, and possibly also in extrapyramidal disorders and migraine (for reviews see e.g. Reynolds, 1979; Wolf and Mosnaim, 1983). Recently, it has been suggested that PEA at least partly mediates the antidepressant effect of map-rotiline (Fawcett et al., 1983).
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Waldmeier, P.C., Buchle, AM., Lauber, J. (1985). Cerebral 2-Phenylethylamine Concentrations and Turnover not Influenced by Various Pharmacological Treatments in Rats. In: Boulton, A.A., Maitre, L., Bieck, P.R., Riederer, P. (eds) Neuropsychopharmacology of the Trace Amines. Humana Press. https://doi.org/10.1007/978-1-4612-5010-4_2
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DOI: https://doi.org/10.1007/978-1-4612-5010-4_2
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