Cited by 271Tryptophan and brain disordersNeurotransmitter Receptor Influence on BehaviorMemory and Neural Mechanisms

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Tryptophan depletion in normal volunteers produces selective impairment in memory consolidation.

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Riedel, W. J., Klaassen, Tineke, Deutz, Nicolaas E. P., van Someren, Astrid, van Praag, Herman M.·1999·Psychopharmacology

DOI 10.1007/s002130050845

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Abstract

Serotonin (5-hydroxytryptamine; 5-HT) circuits may play a role in cognitive performance, particularly in learning and memory. Cognitive impairment is often seen in depressed patients, in whom 5-HT turnover in the brain is thought to be lowered. A possible human pharmacological model to study the involvement of the serotonergic system in cognitive impairment is to reduce central 5-HT synthesis through L-tryptophan depletion in healthy subjects. In this study, the cognitive effects of tryptophan depletion were assessed and whether genetically or developmentally determined vulnerability factors were predictive of the cognitive impairment induced by tryptophan depletion. Sixteen healthy volunteers with a positive family history of depression and 11 without were given 100 g of an amino acid mixture with or without tryptophan, according to a double-blind, cross-over design. Tryptophan depletion specifically impaired long-term memory performance in all subjects: delayed recall performance, recognition sensitivity, and recognition reaction times were significantly impaired after tryptophan depletion relative to placebo. Short-term memory and perceptual and psychomotor functions were unchanged. There were no differences between groups with a positive and a negative family history for depression. On the basis of these results, it is concluded that tryptophan depletion specifically impairs long-term memory formation, presumably as a result of an acute decrease in 5-HT turnover in the brain.

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Authors: Riedel, W. J., Klaassen, T., Deutz, N. E. P., van Someren, A., & van Praag, H. M.
Affiliations: Maastricht University (NL)
ORCID: Riedel, W. J.
Deutz, Nicolaas E. P.
Venue: Psychopharmacology
Publisher: Springer Science and Business Media LLC
Published: 1999-02-01
Volume: 141
Issue: 4
Pages: 362-369
ISSN: 0033-3158 (ISSN-L)
1432-2072
DOI: 10.1007/s002130050845
OpenAlex: W1963545345
Cited by: 271
References: 29
Citations by year: 2026: 1 · 2025: 4 · 2024: 4 · 2023: 4 · 2022: 7 · 2021: 5 · 2020: 4 · 2019: 2 · 2018: 8 · 2017: 5 · 2016: 6 · 2015: 7 · 2014: 7 · 2013: 10 · 2012: 7
FWCI: 5.04
Type: journal article
Language: en
Open access: green
cris.maastrichtuniversity.nl
Licence: other-oa
www.springer.com/tdm (tdm)
Locations: Psychopharmacology (publishedVersion)
PubMed (publishedVersion)
Research Publications (Maastricht University) (submittedVersion, other-oa)
Funders: Universiteit Maastricht
Topics: Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords: tryptophan depletion, serotonin, memory consolidation, long-term memory, cognitive impairment, family history of depression, serotonergic system, depression, recognition memory, delayed recall, healthy volunteers
MeSH terms: Adolescent, Adult, Amino Acids, Cognition, Depressive Disorder, Major, Major Depressive Disorder, Double-Blind Method, Female, Humans, Learning, Male, Memory Disorders, Middle Aged, Sex Characteristics, Tryptophan, Cross-Over Studies

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Tryptophan depletion in normal volunteers produces selective impairment in memory consolidation.

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