Differential effects of 5-HTTLPR genotypes on the behavioral and neural responses to tryptophan depletion in patients with major depression and controls
Abstract
CONTEXT: Tryptophan depletion (TD) is a model used to study the contribution of reduced serotonin transmission to the pathogenesis of major depressive disorder (MDD). Recent studies have not sufficiently addressed the relative contribution of a functional-length triallelic polymorphism in the promoter of the serotonin transporter, 5-HTTLPR, to the behavioral and neural responses to TD in individuals with remitted MDD (rMDD) and controls. OBJECTIVE: To determine the role of 5-HTTLPR on the behavioral and neural responses to TD in medication-free patients with rMDD and individually matched controls. DESIGN: Participants were stratified according to diagnosis and 5-HTTLPR genotypes and underwent TD on one test day and sham depletion on the other test day in a prospective, double-blind, randomized order. SETTING: Outpatient clinic. PARTICIPANTS: Twenty-seven medication-free patients with rMDD (18 women and 9 men) and 26 controls (17 women and 9 men). INTERVENTIONS: Tryptophan depletion was induced by administration of capsules containing an amino acid mixture without tryptophan. Sham depletion used identical capsules containing lactose. Fludeoxyglucose F 18 positron emission tomography was performed 6 hours after TD. Magnetic resonance images were obtained for each participant. MAIN OUTCOME MEASURES: Quantitative positron emission tomography of regional cerebral metabolic rates for glucose and measures of depression using the Hamilton Depression Rating Scale. RESULTS: Behavioral responses to TD are affected by 5-HTTLPR in patients with rMDD and controls. A direct effect of 5-HTTLPR on the regulation of regional cerebral metabolic rates for glucose was identified in patients with rMDD for the amygdala, hippocampus, and subgenual anterior cingulate cortex. CONCLUSIONS: Variations in 5-HTTLPR modulate the sensitivity of patients with rMDD and controls to the behavioral effects of TD. In patients with rMDD, variations in triallelic 5-HTTLPR have a direct effect on regulation of regional cerebral metabolic rates for glucose in a corticolimbic circuit that has been implicated in rMDD.
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In recovered MDD cases who experience depressive relapse under experimental conditions involving serotonin or catecholamine depletion, the metabolic activity increases in these regions as the depressive symptoms return.
“Conversely, in recovered MDD cases who experience depressive relapse under experimental conditions involving serotonin or catecholamine depletion, the metabolic activity increases in these regions as the depressive symptoms return (Neumeister et al. 2004; Hasler et al. 2008) although the elevation of left amygdala activity during serotonin depletion-induced relapse was limited to homozygotes for”
From Brain structural and functional abnormalities in mood disorders: implications for neurocircuitry models of depression (2008) · cites this paper as Neumeister et al. 2006b
Left amygdala activation increases during tryptophan depletion-induced relapses into depression only in MDD patients homozygous for the long allele of the serotonin-transporter polymorphism.
“In addition, activation of the left amygdala increases during relapses into depression induced by tryptophan depletion, but only in MDD patients who are homozygous for the long allele of the serotonin-transporter polymorphism (73).”
From Localization of Dysfunction in Major Depressive Disorder: Prefrontal Cortex and Amygdala (2011) · cites this paper as [73]
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- Authors
- Neumeister, A., Hu, X.-Z., Luckenbaugh, D. A., Schwarz, M., Nugent, A. C., Bonne, O., Herscovitch, P., Goldman, D., Drevets, W. C., & Charney, D. S.
- Affiliations
- Yale University (US)
- ORCID
- Venue
- Archives of General Psychiatry
- Publisher
- American Medical Association (AMA)
- Published
- 2006-09-01
- Volume
- 63
- Issue
- 9
- Pages
- 978
- ISSN
- 0003-990X (ISSN-L)
- OpenAlex
- W2075058568
- Cited by
- 161
- References
- 49
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 4 · 2022: 2 · 2021: 1 · 2020: 3 · 2019: 3 · 2018: 3 · 2017: 1 · 2016: 6 · 2015: 8 · 2014: 11 · 2013: 10 · 2012: 14
- FWCI
- 7.58
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Archives of General Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Health Sciences › Medicine › Pharmacology › Treatment of Major Depression
- Keywords
- 5-HTTLPR, serotonin transporter, tryptophan depletion, major depressive disorder, remitted depression, genetic polymorphism, regional cerebral glucose metabolism, amygdala, hippocampus, subgenual anterior cingulate cortex, corticolimbic circuits, serotonin transmission, gene-environment interaction
- MeSH terms
- Adult, Ambulatory Care, Amino Acids, Brain, Major Depressive Disorder, Double-Blind Method, Female, Genotype, Glucose, Humans, Male, Neural Pathways, Placebos, Prospective Studies, Psychiatric Status Rating Scales, Serotonin, Tissue Distribution, Tryptophan, Fluorodeoxyglucose F18, Polymorphism, Single Nucleotide, Positron-Emission Tomography, Serotonin Plasma Membrane Transport Proteins
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