Abstract
Imbalances in the neuronal homeostasis of the trace amines β-phenylethylamine (PE) and tryptamine (T) have been implicated in the aetiology of certain neuropsychiatry disorders, including depression (Dewhurst, 1984 for review). Tranylcypromine (TCP), a monoamine oxidase (MAO) inhibitor used clinically as an antidepressant, has been shown to elevate substantially brain concentrations of these trace amines (Philips and Boulton, 1979). A number of N-alkylated derivatives of TCP have been synthesized in our laboratories to test them as potential prodrugs of TCP. The prodrug N-(2-cyanoethyl)tranylcypromine (CE-TCP) was found to be a potent MAO inhibitor in its own right (Baker et al., 1984). A neurochemical study is now reported in which the effects of TCP and CE-TCP on brain levels of the trace amines PE and T are compared.
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© 1985 The Human Press Inc.
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Nazarali, A.J., Baker, G.B., Coutts, R.T., Hampson, D.R., Hall, T.W., Micetich, R.G. (1985). Tranylcypromine and an N-Cyanoethyl Analogue: Effects on Brain Levels of the Trace Amines β-Phenylethylamine and Tryptamine. 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_21
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DOI: https://doi.org/10.1007/978-1-4612-5010-4_21
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