The effect of acute tryptophan depletion on the BOLD response during performance monitoring and response inhibition in healthy male volunteers

Evers, Elisabeth A. T.; Veen, Frederik M. van der; Deursen, Jeroen A. van; Schmitt, J.A.J.; Deutz, N.E.P.; Jolles, Jelle

doi:10.1007/s00213-006-0411-6

Cited by 71 publications

(66 citation statements)

References 58 publications

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“…Thus, studies in rats and humans have shown that manipulating 5-HT does not affect performance on tasks of inhibition that have no clear affective component, such as the stop-signal reaction-time task Cools et al, 2005;Chamberlain et al, 2006;Bari et al, 2009;Eagle et al, 2009), the self-ordered spatial working memory task (Walker et al, 2009), and the go-nogo task (Rubia et al, 2005;Evers et al, 2006) (but see LeMarquand et al, 1999).…”

Section: The Coupling Between Inhibitory and Aversive Effects Of Seromentioning

confidence: 99%

Serotonin and Dopamine: Unifying Affective, Activational, and Decision Functions

Cools

Nakamura²,

Daw³

2010

Neuropsychopharmacol

409

369

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Serotonin, like dopamine (DA), has long been implicated in adaptive behavior, including decision making and reinforcement learning. However, although the two neuromodulators are tightly related and have a similar degree of functional importance, compared with DA, we have a much less specific understanding about the mechanisms by which serotonin affects behavior. Here, we draw on recent work on computational models of dopaminergic function to suggest a framework by which many of the seemingly diverse functions associated with both DA and serotoninFcomprising both affective and activational ones, as well as a number of other functions not overtly related to eitherFcan be seen as consequences of a single root mechanism.

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Section: The Coupling Between Inhibitory and Aversive Effects Of Seromentioning

confidence: 99%

Serotonin and Dopamine: Unifying Affective, Activational, and Decision Functions

Cools

Nakamura²,

Daw³

2010

Neuropsychopharmacol

409

369

View full text Add to dashboard Cite

show abstract

“…83 or magnetic resonance imaging (MRI). 33,[42][43][44][45][46]74 Two studies stratified mood response to ATD by genetic polymorphism of the 5-HT transporter promoter region. 65,67 We judged the overall methodological quality of the identified studies as good, with appropriate application of the ATD, APTD or AMPT depletion.…”

Section: Identified Studiesmentioning

confidence: 99%

“…This might be indicative of a biological vulnerability, which is revealed by depletion studies. Of interest are the findings of recent studies that combined ATD with neuroimaging or genetic sampling, 33,[42][43][44][45][46]65,66,67,70,74,83,87,97,103,104,123 reviewed by Fusar-Poli et al 25 The intelligent approach of combining depletion with imaging or genotyping appears very promising. A summary of the complex results of these studies goes beyond the scope of our review.…”

Section: Do Depletion Studies Elucidate the Pathogenesis Of Mdd?mentioning

confidence: 99%

Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion studies

2007

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Dysfunction in the monoamine systems of serotonin (5-HT), norepinephrine (NE) and dopamine (DA) may causally be related to major depressive disorder (MDD). Monoamine depletion studies investigate the direct effects of monoamines on mood. Acute tryptophan depletion (ATD) or para-chlorophenylalanine (PCPA) deplete 5-HT, acute phenylalanine/ tyrosine depletion (APTD) or alpha-methyl-para-tyrosine (AMPT) deplete NE/DA. Available depletion studies found conflicting results in heterogeneous populations: healthy controls, patients with previous MDD in remission and patients suffering from MDD. The decrease in mood after 5-HT and NE/DA depletion in humans is reviewed and quantified. Systematic search of MEDLINE and EMBASE (1966-October 2006) and cross-references was carried out. Randomized studies applying ATD, PCPA, APTD or AMPT vs control depletion were included. Pooling of results by meta-analyses was stratified for studied population and design of the study (within or between subjects). Seventy-three ATD, 2 PCPA, 10 APTD and 8 AMPT studies were identified of which 45 ATD and 8 APTD studies could be meta-analyzed. 5-HT or NE/DA depletion did not decrease mood in healthy controls. 5-HT or NE/DA depletion slightly lowered mood in healthy controls with a family history of MDD. In drug-free patients with MDD in remission, a moderate mood decrease was found for ATD, without an effect of APTD. ATD induced relapse in patients with MDD in remission who used serotonergic antidepressants. In conclusion, monoamine depletion studies demonstrate decreased mood in subjects with a family history of MDD and in drug-free patients with MDD in remission, but do not decrease mood in healthy humans. Although depletion studies usefully investigate the etiological link of 5-HT and NE with MDD, they fail to demonstrate a causal relation. They presumably clarify a vulnerability trait to become depressed. Directions for further investigation of this vulnerability trait are proposed.

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“…Also, acute tryptophan depletion triggered depressive moods in relatives of patients with MDD, but not in healthy controls. 10 For both groups, severity of depressive mood after acute tryptophan depletion was correlated with an activation in the posterior part of the anterior cingulate cortex (ACC) during the Stroop task. 10 In our recent study, the unaffected healthy first-degree relatives of patients with MDD experienced more activation in the left caudate nucleus and the right middle cingulate cortex (MCC) during inhibition of emotional information; we hypothesized that changes in activation may be the result of a mechanism of compensation.…”

Section: Introductionmentioning

confidence: 99%

“…10 For both groups, severity of depressive mood after acute tryptophan depletion was correlated with an activation in the posterior part of the anterior cingulate cortex (ACC) during the Stroop task. 10 In our recent study, the unaffected healthy first-degree relatives of patients with MDD experienced more activation in the left caudate nucleus and the right middle cingulate cortex (MCC) during inhibition of emotional information; we hypothesized that changes in activation may be the result of a mechanism of compensation. 11 Our findings suggested that areas responsible for executive function and emotional processing may be altered in individuals with family history of MDD.…”

Section: Introductionmentioning

confidence: 99%

Recruitment of the left hemispheric emotional attention neural network in risk for and protection from depression

Lisiecka

Carballedo

Fagan

et al. 2013

J Psychiatry Neurosci

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IntroductionIndividuals with a first-degree relative who has major depressive disorder (MDD) are at a 2-to 3-fold greater risk for depression than those without a family history of MDD. 1 Rela tives of depressed patients, compared with individuals without family history of psychiatric disorders, are characterized by elevated neuroticism, depressive cognitions and rigidity 2 and by stability of these traits over time.3 Patients with MDD who had relatives with an affective disorder display greater neuroticism 4 and have an earlier age of onset of MDD. 5 Evidently, family history of MDD alters susceptibility to depression and to an acute MDD episode. The factor is clinically important since it involves mechanisms of elevated risk for MDD (relatives of patients with MDD compared with healthy controls), suggests relative resilience to the disease (relatives of patients with MDD compared with the patients themselves) and points to different endophenotypes of healthy controls and patients with MDD. A good understanding of these mechanisms should not be underestimated if diagnosis, therapy and prevention of the disorder are to be enhanced. Background: Family history of major depressive disorder (MDD) increases individuals' vulnerability to depression and alters the way depression manifests itself. Emotion processing and attention shifting are functions altered by MDD and family history of the disease; therefore, it is important to recognize the neural correlates of these functions in association with both factors. Methods: Our study determines neural correlates of emotion processing and attention shifting for healthy individuals and patients with MDD with and without family history of depression. We compared the performance and neural activity in a functional magnetic resonance imaging experiment examining emotion processing and attention shifting in all participants. Results: Our sample included 4 study groups: healthy controls without family history of depression (n = 25), patients with MDD without family history of the disease (n = 20), unaffected healthy first-degree relatives of patients with MDD (n = 21) and patients with MDD with family history of MDD (n = 30). Compared with healthy controls, unaffected first-degree relatives overactivate the somatosensory cortex and the attention controlling areas during both emotion processing and attention shifting. Patients with family history of MDD have stronger neural activation in subcortical areas during shifting attention from negative stimuli. Patients without family history of MDD have less activation in the paralimbic regions and more activation in core limbic areas, especially during emotion processing. Limitations: The conclusions about the intergroup differences in activation can be drawn only about neural areas engaged in the task. Conclusion: Unaffected first-degree relatives of patients with MDD overreact to external emotional cues and compensate for the vulnerability with increased involvement of executive control. Patients with a family history of MDD have le...

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The effect of acute tryptophan depletion on the BOLD response during performance monitoring and response inhibition in healthy male volunteers

Cited by 71 publications

References 58 publications

Serotonin and Dopamine: Unifying Affective, Activational, and Decision Functions

Serotonin and Dopamine: Unifying Affective, Activational, and Decision Functions

Mood is indirectly related to serotonin, norepinephrine and dopamine levels in humans: a meta-analysis of monoamine depletion studies

Recruitment of the left hemispheric emotional attention neural network in risk for and protection from depression

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