ArticlePloS one2012
Effects of acute tryptophan depletion on brain serotonin function and concentrations of dopamine and norepinephrine in C57BL/6J and BALB/cJ mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
34 citing papers in PubMed, 72 citations in OpenAlex.
- Arbitration between model-free and model-based control is not affected by transient changes in tonic serotonin levels.Journal of psychopharmacology (Oxford, England) · 2024Trial
- Acute tryptophan loading decreases functional connectivity between the default mode network and emotion-related brain regions.Human brain mapping · 2019Trial
- Trial
- Cortico-limbic connectivity in MAOA-L carriers is vulnerable to acute tryptophan depletion.Human brain mapping · 2017Trial
- Effects of a short-term reduction in brain serotonin synthesis on the availability of the soluble leptin receptor in healthy women.Journal of neural transmission (Vienna, Austria : 1996) · 2015Trial
- Serotonin and dopamine differentially affect appetitive and aversive general Pavlovian-to-instrumental transfer.Psychopharmacology · 2015Trial
- Change in electrodermal activity after acute tryptophan depletion associated with aggression in young people with attention deficit hyperactivity disorder (ADHD).Journal of neural transmission (Vienna, Austria : 1996) · 2014Trial
- Acute tryptophan depletion in accordance with body weight: influx of amino acids across the blood-brain barrier.Journal of neural transmission (Vienna, Austria : 1996) · 2012Trial
- Acute tryptophan depletion balances altered resting-state functional connectivity of the salience network in female patients recovered from anorexia nervosa.Journal of psychiatry & neuroscience : JPNTrial
- Plant and animal protein intake and its association with depression, anxiety, and stress among Iranian women.BMC public health · 2023Article
- Direct and indirect mechanisms by which the gut microbiota influence host serotonin systems.Neurogastroenterology and motility · 2022Review
- Article
- Diabetes and Cognitive Impairment: A Role for Glucotoxicity and Dopaminergic Dysfunction.International journal of molecular sciences · 2021Review
- The evolving metabolic landscape of chromatin biology and epigenetics.Nature reviews. Genetics · 2020Review
- Review
- Detection of a High-Turnover Serotonin Circuit in the Mouse Brain Using Mass Spectrometry Imaging.iScience · 2019Article
- Acute Tryptophan Depletion Moja-De: A Method to Study Central Nervous Serotonin Function in Children and Adolescents.Frontiers in psychiatry · 2019Article
- Role of Tryptophan in Microbiota-Induced Depressive-Like Behavior: Evidence From Tryptophan Depletion Study.Frontiers in behavioral neuroscience · 2019Article
- Serotonergic Contributions to Human Brain Aggression Networks.Frontiers in neuroscience · 2019Article
- Article
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute tryptophan depletion (ATD) is a method of lowering brain serotonin (5-HT). Administration of large neutral amino acids (LNAA) limits the transport of endogenous tryptophan (TRP) across the blood brain barrier by competition with other LNAAs and subsequently decreases serotonergic neurotransmission. A recent discussion on the specificity and efficacy of the ATD paradigm for inhibition of central nervous 5-HT has arisen. Moreover, side effects such as vomiting and nausea after intake of amino acids (AA) still limit its use. ATD Moja-De is a revised mixture of AAs which is less nauseating than conventional protocols. It has been used in preliminary clinical studies but its effects on central 5-HT mechanisms and other neurotransmitter systems have not been validated in an animal model. We tested ATD Moja-De (TRP-) in two strains of mice: C57BL/6J, and BALB/cJ, which are reported to have impaired 5-HT synthesis and a more anxious phenotype relative to other strains of mice. ATD Moja-De lowered brain TRP, significantly decreased 5-HT synthesis as indexed by 5-HTP levels after decarboxlyase inhibition, and lowered 5-HT and 5-HIAA in both strains of mice, however more so in C57BL/6J than in BALB/cJ. Dopamine and its metabolites as well as norepinephrine were not affected. A balanced (TRP+) control mixture did not raise 5-HT or 5-HIAA. The present findings suggest that ATD Moja-De effectively and specifically suppresses central serotonergic function. These results also demonstrate a strain-specific effect of ATD Moja-De on anxiety-like behavior.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.