Separation and quantitation of some urinary arylalkylamines

Slingsby, Judy M.; Boulton, Alan A.

doi:10.1016/s0021-9673(00)81101-2

Cited by 37 publications

(8 citation statements)

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“…(1974) to be less than 1 psi24 h. The excretion of mand p-tyramine vary considerably between subjects, hence the different means in the excretions in Table 3. The excretion rate of m-and p-tyramine in man is comparable to those reported in the literature (JEP-SON er al., 1960;PERRY & SCHROEDER, 1963;COWARD er al., 1964;VOGEL et al, 1967;KING et al, 1974;SLINGSBY & BOULTON, 1976). Table 2, the concentrations of the three amines measured did not significantly change 1 h after eating.…”

Section: Discussionmentioning

confidence: 88%

“…Of the various amines that could be derived from the hydroxylation of PEA (BOULTON er al.. 1974u.h) only m-and p-tyramine were detected in measurable amounts in urine. These two isomers of tyramine were previously detected and quantified in human (JEPSON et a/., 1960;PERRY & SCHROEDER, 1963;COWARD et al, 1964;KING et a/., 1974;SLINGSBY & BOULTON, 1976) and rat (BOULTON et a/., 1974~) urines. They have also been found in various animal tissues including the brain (PHILIPS et a/., 1974; BOULTON et a/., 1974a, b ; BOULTON, 1976a, b).…”

Section: Discussionmentioning

confidence: 95%

“…PEA is normally excreted in human urine (JEPSON et al, 1960;OATES et al, 1963;SCHWEITZER et al, 1975) and is present in the brains of a number of animal species (INWANG et al, 1973;MOSNAIM & INWANG, 1973;SAAVEDRA, 1974a;WILLNER et al, 1974;DURDEN et al, 1973;BOULTON et al, 1974b). The concentrations of PEA evaluated by radioenzymatic (SAAVEDRA, 1974a,h), mass spectrometric (WILLNER et a/., 1974;DURDEN et al, 1973;BOULTON et al, 1974a;SLINGSBY & BOULTON, 1976) and recently by a spectrofluoro-Send reprint requests to Dr. F. Karoum. Abbreviations used: PEA, phenylethylamine; MF, mass tragmentography; MID, multiple ion detection; AMU, atomic mass unit; MAO, monoamine oxidase.…”

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confidence: 99%

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MASS FRAGMENTOGRAPHY OF PHENYLETHYLAMINE, m‐ AND p‐TYRAMINE AND RELATED AMINES IN PLASMA, CEREBROSPINAL FLUID, URINE, AND BRAIN

Karoum

Nasrallah

Potkin

et al. 1979

Journal of Neurochemistry

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—A mass fragmentographic method for the assay of phenylethylamine (PEA) and a number of related amines in several biological materials is described. The gas chromatographic column employed for this analysis is a 12ft 1/8 in. o.d. steel column packed with 0.5% OV22+ 2% SE54 + 1% OV210 coated on 80/100 mesh chromosorb W (HP). The mass spectral characteristics of these amines are illustrated, compared, and discussed. Of the various monoamines which could be measured, only PEA, m‐ and p‐tyramine were detected in measurable quantities. Phenylethanolamine and p‐octopamine were found in trace amounts in urine, plasma, cerebrosponal fluid, and rat brain. No diurnal variation in the urinary excretion of PEA, m‐ and p‐tyramine was observed. Plasma concentration of PEA or p‐tyramine did not significantly change 1 h after eating a breakfast. Furthermore, consuming 200 g of Cadbury milk chocolate containing about 1 mg of PEA, 0.1 mg of phenylethanolamine and 10 mg of p‐tyramine did not significantly alter urine excretions of these three amines. In the brain, as has been reported by others, we found that PEA and p‐tyramine are not evenly distributed and that the highest concentrations are found in the hypothalamus and caudate. From the results obtained we concluded that PEA, m‐ and p‐tyramine are probably produced from endogenous sources and that the direct contribution of diet to their urine excretion is small.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 95%

mentioning

confidence: 99%

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MASS FRAGMENTOGRAPHY OF PHENYLETHYLAMINE, m‐ AND p‐TYRAMINE AND RELATED AMINES IN PLASMA, CEREBROSPINAL FLUID, URINE, AND BRAIN

Karoum

Nasrallah

Potkin

et al. 1979

Journal of Neurochemistry

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“…Scientists are still attempting to explain the delayed onset of clinical improvement despite the immediate changes in neuroenvironment (e.g., inhibition of uptake of 5-HT and/ or NE) produced by antidepressants, but downregulation of receptors for biogenic amines is thought to account, at least in part, for the delayed therapeutic efficacy of antidepressant drugs. Tryptamine has been implicated in the etiology of a variety of psychiatric illnesses, including the affective disorders [Dewhurst, 1968a,b;Slingsby and Boulton, 1976;Mousseau, 1993]. Tryptamine has been implicated in the etiology of a variety of psychiatric illnesses, including the affective disorders [Dewhurst, 1968a,b;Slingsby and Boulton, 1976;Mousseau, 1993].…”

Section: Resultsmentioning

confidence: 99%

4‐fluorotranylcypromine, a novel monoamine oxidase inhibitor: Neurochemical effects in rat brain after short‐ and long‐term administration

1999

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A series of acute and chronic experiments was conducted on 4-fluorotranylcypromine (FTCP), an analog of the monoamine oxidase (MAO)-inhibiting antidepressant tranylcypromine (TCP) in which the 4 position of the phenyl ring is protected from metabolism. These studies demonstrated that FTCP is a more potent inhibitor of MAO ex vivo than is the parent drug. Despite its similarity in structure to pchloroamphetamine, FTCP does not cause a depletion of brain levels of 5-hydroxytryptamine (5-HT) after chronic administration; in fact, it increases brain 5-HT to levels similar to those produced by TCP. After chronic administration, FTCP produces a downregulation of β-adrenergic and tryptamine receptors, in common with TCP and several other antidepressants. Pretreatment of rats with iprindole or trifluperazine, drugs known to block cytochrome P450-mediated hydroxylation reactions and to elevate brain levels of TCP, had no effects on FTCP brain levels, suggesting that metabolic drug-drug interactions may be less of a concern with FTCP than with TCP. In vitro uptake experiments in prisms prepared from hypothalamus or striatum revealed that TCP and FTCP are both potent inhibitors of norepinephrine (NE) uptake; FTCP is a more potent inhibitor of 5-HT uptake than is TCP. FTCP is a more potent releaser of 5-HT than is TCP. Drug Dev.

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“…Tryptamine is an endogenous neuroactive metabolite of tryptophan with behavioral, physiological, and pharmacological effects (Mousseau, 1993) . Numerous reports implicate disturbances in the synthesis and metabolism of tryptamine in the cause of certain neuropsychiatric disorders including depression, Parkinson's disease, schizophrenia, and Tourette's syndrome (Saavedra and Axelrod, 1972;Slingsby and Boulton, 1976 ;Baker et al, 1993 ;Goodnough et al, 1993 ;see Mousseau, 1993, for review function of this amine in such disorders, however, is restricted to extrapolation from studies derived from animal models or from work with peripheral tissue or fluid samples from affected patients . The feasibility of a role for tryptamine in psychopathology (Dewhurst, 1968) was strengthened by studies of [3 H]tryptamine binding sites in rat brain (Kellar and Cascio, 1982;Wood et al ., 1984;Altar et al, 1986;Nguyen and Juorio, 1989a) .…”

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confidence: 99%

The [³H]Tryptamine Receptor in Human Brain: Kinetics, Distribution, and Pharmacologic Profile

Mousseau

Butterworth

1994

Journal of Neurochemistry

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The kinetics and distribution of [3H]tryptamine binding sites in human brain were investigated. Specific [3H]tryptamine binding in frontal cortex was of nanomolar affinity, reversible, saturable, and best fit to a single‐site model. A heterogeneous distribution for this binding site was demonstrated, with the highest density observed in hippocampus, thalamus ≫ caudate nucleus, frontal cortex, pons, temporal cortex > globus pallidus/putamen, cerebellum. The similarities in kinetics and distribution of the [3H]tryptamine binding site in human and rat brain indicate that these two binding sites represent homologous structures. However, the present displacement studies using various ligands (indoleamines and other tryptophan metabolites, phenylethylamines, and miscellaneous drugs) and salts (Na+, K+, Ca2+, Mg2+, Cu2+) indicate stereospecific displacement as well as a rank‐order potency profile that is different from that reported for the rat [3H]tryptamine binding site. This suggests the presence of distinct species‐dependent [3H]tryptamine binding site subtypes. Taken together with the documented electrophysiological and behavioral evidence of tryptamine‐mediated effects in the rat and the recent report of a significant loss of these binding sites in human portal systemic encephalopathy, as well as the present demonstration of an effect of guanine nucleotides on [3H]‐tryptamine binding affinity, these findings suggest that these binding sites might be functional receptors. The implied role of tryptamine in neuropsychiatric disorders is supported by this demonstration of a receptor for [3H]‐tryptamine in human brain.

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Separation and quantitation of some urinary arylalkylamines

Cited by 37 publications

References 25 publications

MASS FRAGMENTOGRAPHY OF PHENYLETHYLAMINE, m‐ AND p‐TYRAMINE AND RELATED AMINES IN PLASMA, CEREBROSPINAL FLUID, URINE, AND BRAIN

MASS FRAGMENTOGRAPHY OF PHENYLETHYLAMINE, m‐ AND p‐TYRAMINE AND RELATED AMINES IN PLASMA, CEREBROSPINAL FLUID, URINE, AND BRAIN

4‐fluorotranylcypromine, a novel monoamine oxidase inhibitor: Neurochemical effects in rat brain after short‐ and long‐term administration

The [³H]Tryptamine Receptor in Human Brain: Kinetics, Distribution, and Pharmacologic Profile

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Separation and quantitation of some urinary arylalkylamines

Cited by 37 publications

References 25 publications

MASS FRAGMENTOGRAPHY OF PHENYLETHYLAMINE, m‐ AND p‐TYRAMINE AND RELATED AMINES IN PLASMA, CEREBROSPINAL FLUID, URINE, AND BRAIN

MASS FRAGMENTOGRAPHY OF PHENYLETHYLAMINE, m‐ AND p‐TYRAMINE AND RELATED AMINES IN PLASMA, CEREBROSPINAL FLUID, URINE, AND BRAIN

4‐fluorotranylcypromine, a novel monoamine oxidase inhibitor: Neurochemical effects in rat brain after short‐ and long‐term administration

The [3H]Tryptamine Receptor in Human Brain: Kinetics, Distribution, and Pharmacologic Profile

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The [³H]Tryptamine Receptor in Human Brain: Kinetics, Distribution, and Pharmacologic Profile