The role of serotonin in reward, punishment and behavioural inhibition in humans: Insights from studies with acute tryptophan depletion

2014 ◽  
Vol 46 ◽  
pp. 365-378 ◽  
Author(s):  
Paul Faulkner ◽  
J.F. William Deakin
Keyword(s):  
Acute Tryptophan Depletion ◽  
Tryptophan Depletion ◽  
Behavioural Inhibition

scholarly journals Evaluating the role of serotonin in hot flashes after breast cancer using acute tryptophan depletion

2009 ◽  
Vol 16 (4) ◽  
pp. 644-652 ◽  
Author(s):  
Janet S. Carpenter ◽  
Menggang Yu ◽  
Jingwei Wu ◽  
Diane Von Ah ◽  
Jennifer Milata ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Hot Flashes ◽  
Acute Tryptophan Depletion ◽  
Tryptophan Depletion

scholarly journals Evaluating the Role of Serotonin on Neuropsychological Function After Breast Cancer Using Acute Tryptophan Depletion

2010 ◽  
Vol 14 (1) ◽  
pp. 5-15 ◽  
Author(s):  
Diane Von Ah ◽  
Todd Skaar ◽  
Fredrick Unverzagt ◽  
Menggang Yu ◽  
Jingwei Wu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cognitive Dysfunction ◽  
Breast Cancer Survivors ◽  
Critical Role ◽  
Acute Tryptophan Depletion ◽  
Common Side Effect ◽  
Tryptophan Depletion ◽  
Motor Speed ◽  
Information Processing Speed

Although cognitive dysfunction is a prevalent and disruptive problem for many breast cancer survivors (BCSs), little research has examined its etiology. One potential mechanism that remains to be explored is serotonin. Serotonin has been implicated in normal and dysfunctional cognitive processes, and serotonin levels are significantly affected by estrogen withdrawal, a common side effect of breast cancer treatment. However, no study has evaluated serotonin’s role on cognitive dysfunction in BCSs. The purpose of this study was to examine the role of serotonin in cognitive dysfunction in survivors by lowering central serotonin concentrations via acute tryptophan depletion (ATD). Based on previous research in noncancer populations, we hypothesized that alterations in central serotonin levels would induce cognitive dysfunction in these women controlling for confounding characteristics such as fluctuating mood and glucose levels. Secondarily, we explored whether genetic variations in serotonin genes would partly explain ATD. Participants included 20 female BCSs, posttreatment for nonmetastatic breast cancer, who received ATD or control in a double-blind, crossover design. Cognitive performance was measured at the 5-hr tryptophan/serotonin nadir on each test day using standardized neuropsychological tests. Specific impairment was noted in episodic memory (delayed recall) and motor speed during ATD versus control. ATD did not alter new learning (immediate recall), working memory, verbal fluency, or information processing speed. Findings suggest that serotonin may play a critical role in memory consolidation and motor functioning in BCSs.

Acute Tryptophan Depletion. Part I: Rationale and Methodology

2005 ◽  
Vol 39 (7) ◽  
pp. 558-564 ◽  
Author(s):  
Sean D. Hood ◽  
Caroline J. Bell ◽  
David J. Nutt
Keyword(s):  
Clinical Experience ◽  
Experimental Technique ◽  
Experimental Work ◽  
Human Subjects ◽  
Acute Tryptophan Depletion ◽  
Tryptophan Depletion ◽  
Valid Method ◽  
Psychiatric Conditions

Objective: Acute tryptophan depletion (ATD) is an experimental technique that has been widely used over the last decade to investigate the role of serotonin (5-HT) in a variety of disorders. This review, the first of two articles, describes the rationale behind this technique and provides detail on how it is applied in research settings. Method: The authors outline the development of this technique with reference to the seminal literature and more recent findings from neuroimaging and neuroendocrine studies. This is supplemented by the authors' clinical experience of over 5 years of continuous experimental work with this paradigm in over 50 subjects. Results: Acute tryptophan depletion is a method that significantly reduces central 5-HT in human subjects. Non-serotonergic explanations of the effects of ATD have not been confirmed, supporting the specificity of this method. Conclusions: The ATD technique is a valid method of manipulating central 5-HT levels. The second article in this series will review the application of ATD in depression, anxiety and other psychiatric conditions.

scholarly journals Oxytocinergic modulation of threat-specific amygdala sensitization in humans is critically mediated by serotonergic mechanisms

2020 ◽  
Author(s):  
Congcong Liu ◽  
Chunmei Lan ◽  
Keshuang Li ◽  
Feng Zhou ◽  
Shuxia Yao ◽  
...  
Keyword(s):  
Therapeutic Potential ◽  
Acute Tryptophan Depletion ◽  
Placebo Control ◽  
Tryptophan Depletion ◽  
Social Emotional ◽  
Double Blind ◽  
Link Type ◽  
Parallel Group ◽  
Emotional Effects

AbstractBackgroundOverarching conceptualizations propose that the complex social-emotional effects of oxytocin (OXT) in humans are partly mediated by interactions with other neurotransmitter systems. Recent animal models suggest that the anxiolytic effects of OXT are critically mediated by the serotonin (5-HT) system, yet direct evidence in humans is lacking.MethodsTo determine the role of 5-HT in OXT-induced attenuation of amygdala threat reactivity and sensitization/ desensitization, we conducted a parallel-group randomized placebo-controlled double-blind experiment during which n = 121 healthy subjects underwent a transient decrease in 5-HT signaling via acute tryptophan depletion (ATD, TRYP-) or the corresponding placebo-control protocols before the administration of intranasal OXT or placebo intranasal spray, respectively. Mean and repetition-dependent changes in threat-specific amygdala reactivity towards threatening stimuli (angry faces) as assessed by fMRI served as the primary outcome.ResultsNo treatment main or interaction effects on amygdala threat reactivity were observed, yet OXT switched bilateral amygdala threat sensitization to desensitization and this effect was significantly attenuated during decreased central 5-HT signaling via pretreatment with TRYP-.ConclusionsThe present findings provide the first evidence for a role of OXT in threat-specific amygdala desensitization in humans and suggest that these effects are critically mediated by the 5-HT system. OXT may have a therapeutic potential to facilitate amygdala desensitization and adjunct up-regulation of 5-HT neurotransmission may facilitate OXT’s anxiolytic potential.The trial was preregistered on clinicaltrials.gov (https://clinicaltrials.gov/ct2/show/NCT03426176, ID NCT03426176)

The role of serotonin for gastrointestinal symptoms: Acute tryptophan depletion increases nausea

2009 ◽  
Vol 47 (09) ◽  
Author(s):  
P Enck ◽  
D Mitschler ◽  
V Schumacher ◽  
EM Muth ◽  
N Rieber ◽  
...  
Keyword(s):  
Gastrointestinal Symptoms ◽  
Acute Tryptophan Depletion ◽  
Tryptophan Depletion

scholarly journals Effect of acute tryptophan depletion on CO2-induced anxiety in patients with panic disorder and normal volunteers

2000 ◽  
Vol 176 (2) ◽  
pp. 182-188 ◽  
Author(s):  
H. E. J. Miller ◽  
J. F. W. Deakin ◽  
I. M. Anderson
Keyword(s):  
Panic Disorder ◽  
Panic Attacks ◽  
Acute Tryptophan Depletion ◽  
Tryptophan Depletion ◽  
Double Blind ◽  
Normal Volunteers ◽  
Plasma Tryptophan ◽  
Drug Free ◽  
Normal Controls

BackgroundUncertainties remain about the role of serotonin in the aetiology and treatment of panic disorder.AimsTo investigate the effect of reducing brain serotonin function on anxiety at rest, and following 5% CO2 provocation in normal controls and patients with panic disorder.MethodTwenty drug-free patients with DSM–III–R panic disorder and 19 controls received a tryptophan-free amino acid drink on one occasion and a control drink on the other in a double-blind, balanced protocol. 5% CO2 was given as a panic challenge after 270 minutes.ResultsPlasma tryptophan fell by more than 80% both patients and controls after the tryptophan-free drink. Tryptophan depletion did not alter resting anxiety. In patients alone, tryptophan depletion caused a greater anxiogenic response and an increased rate of panic attacks (9 v. 2, P<0.05) after 5% CO2 challenge. No normal volunteers panicked.ConclusionsSerotonin may directly modulate panic anxiety in patients with panic disorder. This may underlie the efficacy of serotonergic antidepressants in treating panic disorder.

scholarly journals Effects of lowered serotonin transmission on cocaine-induced striatal dopamine response: PET [11C]raclopride study in humans

2011 ◽  
Vol 199 (5) ◽  
pp. 391-397 ◽  
Author(s):  
Sylvia M. L. Cox ◽  
Chawki Benkelfat ◽  
Alain Dagher ◽  
J. Scott Delaney ◽  
France Durand ◽  
...  
Keyword(s):  
Substance Use ◽  
Substance Use Disorders ◽  
Striatal Dopamine ◽  
Emission Tomography ◽  
Acute Tryptophan Depletion ◽  
Tryptophan Depletion ◽  
Comorbid Conditions ◽  
Drug Craving ◽  
Positron Emission ◽  
Wide Range

BackgroundLow serotonin transmission is thought to increase susceptibility to a wide range of substance use disorders and impulsive traits.AimsTo investigate the effects of lowered serotonin on cocaine-induced (1.0 mg/kg cocaine, self-administered intranasally) dopamine responses and drug craving.MethodIn non-dependent cocaine users, serotonin transmission was reduced using the acute tryptophan depletion method. Striatal dopamine responses were measured using positron emission tomography with [11C]raclopride.ResultsAcute tryptophan depletion increased drug craving and striatal dopamine responses to cocaine. These acute tryptophan depletion-induced increases did not occur in the absence of cocaine.ConclusionsThe results suggest that low serotonin transmission can increase dopaminergic and appetitive responses to cocaine. These findings might identify a mechanism by which individuals with low serotonin are at elevated risk for both substance use disorders and comorbid conditions.

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