Tranylcypromine and an N-Cyanoethyl Analogue: Effects on Brain Levels of the Trace Amines β-Phenylethylamine and Tryptamine

Nazarali, Adil J.; Baker, Glen B.; Coutts, Ronald T.; Hampson, David R.; Hall, T. W.; Micetich, Ronald G.

doi:10.1007/978-1-4612-5010-4_21

Cited by 1 publication

(2 citation statements)

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“…TCP injection in the rat model, TA levels in both hippocampus and diencephalon peaked after roughly 45-90 min. Similarly, Nazarali et al (1985) observed maximum PEA concentrations (control value times 45) in rat brains 120 min after i.p. TCP injection, while maximum TRYP concentrations (control value times 175) took 240 min to manifest.…”

Section: Framing the Discussionmentioning

confidence: 56%

“…There is a paucity of information on TCP metabolism: phase 1 metabolites are known to include p-hydroxytranylcypromine (Nazarali et al 1985), N-acetyltranylcypromine, and N-acetyl-p-hydroxytranylcypromine, while phase 2 metabolites remain unknown (Ulrich et al 2017). TCP is unique among MAOIs in that it is molecularly similar to amphetamine (Ulrich et al 2020); it was initially synthesized by Burger and Yost in 1946 (trans-2-phenylcyclopropylamine) as a close analogue to amphetamine (Abdel-Aleem et al 1998) but was swiftly dismissed (to be later rediscovered as a potent MAOI) due to its low amphetaminergic activity (Ulrich et al 2017): Sherry et al (2000) reported that 'at usual doses of TCP', cyclopropyl ring-opening (a requisite step in the potential formation of amphetamine from TCP) does not significantly occur.…”

Section: Tcp: Select Topics Of Metabolismmentioning

confidence: 99%

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The trace amine theory of spontaneous hypertension as induced by classic monoamine oxidase inhibitors

Eynde¹

2021

J Neural Transm

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The classic monoamine oxidase inhibitors (MAOIs) tranylcypromine (TCP) and phenelzine (PLZ) are powerful antidepressants that come with an equally powerful stigma, and are thus rarely prescribed-despite their well-established effectiveness. Some of these preconceptions appear to stem from unclarity, as the etiology of a rare but important side effect, 'spontaneous hypertension' (SH)-a significant increase in blood pressure absent dietary tyramine ingestion-remains improperly elucidated. This paper aims at uprooting some of the stigma surrounding MAOIs by advancing the trace amine (TA) theory as the causative underpinning of SH. This theory posits that SH results from the considerable influx of TAs observed following TCP-or PLZ-administration. TAs are known, albeit at greatly supraphysiological levels, to raise blood pressure on account of their propensity to exert potent indirect sympathomimetic effects; additionally, some research posits that TAs may induce vasoconstrictive effects partly or wholly separate therefrom, which would then constitute a second hypertensive mechanism. TAs are endogenous to the human body in low quantities. Both TCP and PLZ cause marked elevations of 2-phenylethylamine (PEA), meta-and para-tyramine (m-/p-TYR), octopamine (OA), and tryptamine (TRYP), following both acute and (sub) chronic administration. This paper holds that TYR plays a pivotal role in causing SH, due to its strong pressor effect. Cautious treatment of SH is advised, given its typically self-limiting nature. The risk of hypotensive overshoots must be taken into account. For severe cases, this paper urges reconsideration, following suitable confirmation trials, of antipsychotics (notably risperidone) as these agents may reduce striatal p-TYR levels.

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Section: Framing the Discussionmentioning

confidence: 56%