Neuroendocrine effects of l-tryptophan and dexamethasone

Träskman‐Bendz, Lil; Haskett, Roger F.; Zis, Athanasios P.

doi:10.1007/bf00175195

Cited by 18 publications

(16 citation statements)

References 27 publications

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“…1987). The introduction of new, highly specific drugs for the modula- L-Trp administration, however, fails to rise circulating cortisol levels (Wootf and Lee 1976;Tr/iskman-Bendz et al 1986;Winkour et al 1986). Another example is the effect of Trp on sleep.…”

Section: Discussionmentioning

confidence: 97%

The metabolic fate of infusedl-tryptophan in men: possible clinical implications of the accumulation of circulating tryptophan and tryptophan metabolites

et al. 1992

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L-Tryptophan (Trp) was widely used as a natural tool for the support of serotonin-mediated brain functions and as a challenge probe for the assessment of serotonin-mediated neuroendocrine responses. The metabolic fate of the administered Trp and the kinetics of the accumulation of Trp metabolites in the circulation, however, have never thoroughly been investigated. This study describes the time- and dose-dependent alterations in the plasma levels of various Trp metabolites and large neutral amino acids after the infusion of Trp to healthy young men (1, 3 and 5 g; placebo-controlled, double-blind, cross-over study during day- and night-time). The major Trp metabolites (kynurenine, indole acetic acid and indole lactic acid) in plasma increased dose-dependently but rather slowly after Trp administration to reach their maximal plasma levels (up to 10-fold after the 5 g dose) at about 3 h p.i., and remained at an elevated level (about 5-fold) for up to 8 h. N-acetyl-Trp and 5-hydroxy-Trp rose rapidly and massively after Trp infusions, at the 5 g dose more than 200- and 20-fold, respectively, and declined rapidly to about 5-fold baseline levels within 2 h. Whole blood serotonin levels were almost unaffected by the Trp infusions. A rather slow increase of 5-hydroxyindole acetic acid was seen, reaching maximum values (3-fold at the 5 g dose) at about 2 h after the infusion of Trp. Additionally, a dose-dependent rise of circulating melatonin was observed after L-Trp infusions. The administration of L-Trp caused a depletion of the concentrations of the other large neutral amino acids and a dose dependent decrease of the ratio between plasma tyrosine and the sum of the plasma concentrations of the other large neutral amino acids. Apparently, none of the existing pathways of peripheral Trp metabolism is saturated by its substrate, Trp in men. At least some of the central effects reported after L-Trp administration may be mediated by the Trp-stimulated formation of neuroactive metabolites or by the decreased availability of tyrosine for catecholamine synthesis.

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Section: Discussionmentioning

confidence: 97%

The metabolic fate of infusedl-tryptophan in men: possible clinical implications of the accumulation of circulating tryptophan and tryptophan metabolites

et al. 1992

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“…The e¤ects of the synthetic corticosteroid dexamethasone on the response to L-TRP has previously been examined in normal volunteers (Traskman-Bendz et al 1986). In contrast to our data, an increase in PRL response, but no e¤ect on GH response, to L-TRP infusion was seen following pre-treatment with dexamethasone 1 mg 10 h before infusion.…”

Section: Discussionmentioning

confidence: 99%

5-Hydroxytryptamine receptor function in humans is reduced by acute administration of hydrocortisone

et al. 1998

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5-Hydroxytryptamine1A (5-HT1A) receptors have been shown to be suppressed by corticosteroid hormones in a variety of animal experimental paradigms. It has been suggested that this effect may be central to the pathophysiology of severe clinical depressive illness, a condition in which 5-HT1A receptor function is reduced and corticosteroid hormones are elevated. We report the effects of acute administration of hydrocortisone in normal volunteers on a neuroendocrine model of 5-HT1A receptor function. Fifteen healthy male volunteers took part in a random order, double blind, placebo controlled study, in which 100 mg hydrocortisone or placebo was administered 11 h before infusion of L-tryptophan (L-TRP). Pre-treatment with hydrocortisone significantly reduced the growth hormone (GH), but not the prolactin (PRL) response to the infusion. These data are consistent with the view that acute administration of corticosteroid hormones significantly impairs 5-HT1A receptor mediated function in healthy human volunteers and are in line with animal studies of the effects of corticosteroid hormones on 5-HT1A receptors. We propose that this finding is relevant to the pathophysiological processes which cause severe depressive illness.

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“…Previously, it has been shown that when dexamethasone is given in a dose of 1 mg (in the same paradigm used in our study with hydrocortisone; Porter et al 1998), the PRL response to L-TRP is enhanced but the GH response is not (Traskman-Bendz et al 1986). However, this dose of dexamethasone is well below that which is clinically equipotent to the dose of 100 mg hydrocortisone employed in our study.…”

Section: Introductionmentioning

confidence: 91%

Effects of dexamethasone on neuroendocrine and psychological responses to L-tryptophan infusion

Porter¹,

McAllister-Williams²,

Jones³

et al. 1999

Psychopharmacology

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Neuroendocrine effects of l-tryptophan and dexamethasone

Cited by 18 publications

References 27 publications

The metabolic fate of infusedl-tryptophan in men: possible clinical implications of the accumulation of circulating tryptophan and tryptophan metabolites

The metabolic fate of infusedl-tryptophan in men: possible clinical implications of the accumulation of circulating tryptophan and tryptophan metabolites

5-Hydroxytryptamine receptor function in humans is reduced by acute administration of hydrocortisone

Effects of dexamethasone on neuroendocrine and psychological responses to L-tryptophan infusion

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