The Effects of Precursor Loading in the Cerebral Metabolism of 5‐hydroxyindoles

Moir, A. T. B.; Eccleston, D.

doi:10.1111/j.1471-4159.1968.tb06827.x

Cited by 394 publications

(96 citation statements)

References 25 publications

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“…These findings and recent experiments concerning the relation of cerebral 5-hydroxytryptamine to a syndrome of hyperactivity and hyperpyrexia (Grahame-Smith, 1971) would suggest that the model previously proposed for cerebral 5-hydroxytryptamine metabolism (Moir & Eccleston, 1968) should be modified. The diagram shown in Fig.…”

Section: Discussionmentioning

confidence: 96%

Interaction in the cerebral metabolism of the biogenic amines. Effects of phenelzine on the cerebral metabolism of the 5‐hydroxyindoles in dog brain

Moir

1972

British J Pharmacology

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Summary Chronic administration of phenelzine to dogs caused 5‐hydroxyindol‐3‐ylacetic acid (5‐HIAA) concentrations in c.s.f. from the lateral ventricle to be maintained at 50% of their normal values, but did not alter the concentrations of 5‐HIAA in c.s.f. from the cisterna magna. Following 10 days treatment with phenelzine, the active transport of 5‐HIAA from c.s.f. which normally occurs in the region of the fourth ventricle, was inhibited. This transport system was also inhibited by the addition of phenylacetic acid, the acid metabolite of phenelzine, to the fluid perfusing the cerebral ventricles. After 10–12 days treatment with phenelzine all regions of brain showed concentration increases to approximately 300% for 5‐HT and 150% for 5‐HIAA, but no alteration in the tryptophan concentration. Intravenous administration of tryptophan to dogs pretreated with phenelzine caused large increases in the concentration of tryptophan in brain and body fluids but did not alter either the concentrations of 5‐hydroxytryptamine and 5‐HIAA in brain or of 5‐HIAA in c.s.f. A model of the cerebral metabolism of 5‐hydroxytryptamine is proposed and the results are interpreted to mean that phenelzine has inhibitory actions, either directly or in some instances indirectly, on intracerebral tryptophan 5‐hydroxylase, monoamine oxidase and the transport of 5‐HIAA from both brain and c.s.f.

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Section: Discussionmentioning

confidence: 96%

Interaction in the cerebral metabolism of the biogenic amines. Effects of phenelzine on the cerebral metabolism of the 5‐hydroxyindoles in dog brain

Moir

1972

British J Pharmacology

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“…These enzymes catalyze the initial and rate-limiting steps in 5HT and catecholamine synthesis, respectively (Kaufman 1974). Consequently, the synthesis rate in the each pathway is stimulated in vivo by the administration of the appropriate precursor (TRP or TYR) (Moir and Eccleston 1968;Fernstrom and Wurtman 1971;Fernstrom 1983). Generally, however, increases in 5HT synthesis in response to TRP administration are more readily apparent than increases in DA or NE synthesis following TYR administration (Fernstrom 1983 (Carlsson and Lindqvist 1978)].…”

Section: Discussionmentioning

confidence: 99%

Oral branched-chain amino acid supplements that reduce brain serotonin during exercise in rats also lower brain catecholamines

et al. 2013

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Exercise raises brain serotonin release and is postulated to cause fatigue in athletes; ingestion of branched-chain amino acids (BCAA), by competitively inhibiting tryptophan transport into brain, lowers brain NOT THE PUBLISHED VERSION; this is the author's final, peer-reviewed manuscript. The published version may be accessed by following the link in the citation at the bottom of the page.Amino Acids, Vol. 45, No. 5 (November 2013): pg. 1133-1142. DOI. This article is © Springer and permission has been granted for this version to appear in e-Publications@Marquette. Springer does not grant permission for this article to be further copied/distributed or hosted elsewhere without the express permission from Springer.2 tryptophan uptake and serotonin synthesis and release in rats, and reputedly in humans prevents exercise-induced increases in serotonin and fatigue. This latter effect in humans is disputed. But BCAA also competitively inhibit tyrosine uptake into brain, and thus catecholamine synthesis and release. Since increasing brain catecholamines enhances physical performance, BCAA ingestion could lower catecholamines, reduce performance and thus negate any serotonin-linked benefit. We therefore examined in rats whether BCAA would reduce both brain tryptophan and tyrosine concentrations and serotonin and catecholamine synthesis. Sedentary and exercising rats received BCAA or vehicle orally; tryptophan and tyrosine concentrations and serotonin and catecholamine synthesis rates were measured 1 h later in hypothalamus. BCAA reduced hypothalamic tryptophan and tyrosine concentrations, and serotonin and catecholamine synthesis. These reductions in tyrosine concentrations and catecholamine synthesis, but not tryptophan or serotonin synthesis, could be prevented by co-administering tyrosine with BCAA. Complete essential amino acid mixtures, used to maintain or build muscle mass, were also studied, and produced different effects on hypothalamic tryptophan and tyrosine concentrations and serotonin and catecholamine synthesis. Since pharmacologically increasing brain catecholamine function improves physical performance, the finding that BCAA reduce catecholamine synthesis may explain why this treatment does not enhance physical performance in humans, despite reducing serotonin synthesis. If so, adding tyrosine to BCAA supplements might allow a positive action on performance to emerge.

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“…Total plasma tryptophan, as well as the tryptophan/CAA ratio, are indicators for the availability of tryptophan to the brain (Fernstrom 1984) and, hence, for 5-HT synthesis in the brain (Moir and Eccleston 1968).…”

Section: Serotonin (5-ht)mentioning

confidence: 99%

Peripheral Markers of Serotonergic and Noradrenergic Function in Post-Pubertal, Caucasian Males with Autistic Disorder

Croonenberghs

Delmeire²,

Verkerk³

et al. 2000

Neuropsychopharmacology

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Some studies have suggested that disorders in the peripheral and central metabolism of serotonin (5-HT) and noradrenaline may play a role in the pathophysiology of autistic disorder. This study examines serotonergic and noradrenergic markers in a study(5-15 per 10.000) and is four times more common in boys than in girls. Research on the biological pathophysiology of autism has found some evidence for a role of the turnover of serotonin (5-HT) and catecholamines.

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The Effects of Precursor Loading in the Cerebral Metabolism of 5‐hydroxyindoles

Cited by 394 publications

References 25 publications

Interaction in the cerebral metabolism of the biogenic amines. Effects of phenelzine on the cerebral metabolism of the 5‐hydroxyindoles in dog brain

Interaction in the cerebral metabolism of the biogenic amines. Effects of phenelzine on the cerebral metabolism of the 5‐hydroxyindoles in dog brain

Oral branched-chain amino acid supplements that reduce brain serotonin during exercise in rats also lower brain catecholamines

Peripheral Markers of Serotonergic and Noradrenergic Function in Post-Pubertal, Caucasian Males with Autistic Disorder

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