Influence of acute tryptophan depletion on gastric sensorimotor function in humans

2011 ◽  
Vol 300 (2) ◽  
pp. G228-G235 ◽  
Author(s):  
Brecht Geeraerts ◽  
Lukas Van Oudenhove ◽  
Werend Boesmans ◽  
Rita Vos ◽  
Pieter Vanden Berghe ◽  
...  

Peripheral serotonin (5-hydrodytryptamine; 5-HT) is involved in the regulation of gastrointestinal motility and sensation, whereas centrally it plays a role in mood regulation. A dysfunctional serotonergic system may provide a plausible link between functional dyspepsia symptoms and its high psychosocial comorbidity such as anxiety and depression. The aim of this study was to evaluate the effect of decreased 5-HT synthesis by acute tryptophan depletion (ATD) on gastric sensorimotor function and nutrient tolerance, anxiety scores, and gastrointestinal mucosal 5-HT concentrations in healthy volunteers. All subjects were studied under a control condition and during ATD. Gastric sensorimotor function and nutrient tolerance were assessed using a barostat ( n = 16, mean age 28.8 ± 1.4 yr) and a satiety drinking test ( n = 13, mean age 27.3 ± 1.4 yr). Anxiety during the barostat was evaluated using State-Trait Anxiety Inventory (STAI) questionnaire. 5-HT concentrations were measured in fundic and duodenal mucosal biopsies by means of ELISA and immunohistochemistry. ATD significantly decreased plasma tryptophan levels compared with control in every experiment. ATD did not affect gastric sensitivity and compliance but decreased the sensation of nausea during balloon distension (AUC: 17.4 ± 4.3 vs. 11.4 ± 3.4 mm·mmHg, P = 0.030). ATD enhanced the postprandial volume increase (ANOVA, P < 0.05), but this was not accompanied by augmented nutrient tolerance (848 ± 110 vs. 837 ± 99 ml, nonsignificant). ATD had no effect on STAI state anxiety scores. No evidence was found for an effect on the number of enterochromaffin cells, but ATD reduced 5-HT levels in the duodenal mucosa. ATD alters gastric postprandial motor function and distension-induced nausea. These findings confirm involvement of 5-HT in the control of gastric accommodation and sensitivity.

2004 ◽  
Vol 178 (1) ◽  
pp. 92-99 ◽  
Author(s):  
E. A. T. Evers ◽  
D. E. Tillie ◽  
F. M. van der Veen ◽  
C. K. Lieben ◽  
J. Jolles ◽  
...  

2004 ◽  
Vol 177 (1-2) ◽  
pp. 238-238
Author(s):  
E. A. T. Evers ◽  
D. E. Tillie ◽  
F. M. van der Veen ◽  
C. K. Lieben ◽  
J. Jolles ◽  
...  

2000 ◽  
Vol 177 (5) ◽  
pp. 447-451 ◽  
Author(s):  
J. H. Hughes ◽  
F. Dunne ◽  
A. H. Young

BackgroundPrevious studies suggest that brain serotonin neurotransmission may mediate the actions of lithium carbonate. Acute tryptophan depletion reduces brain serotonin and allows the study of this neurotransmitter in patient groups.AimsTo examine the effects of acute tryptophan depletion on mood and suicidal ideation in bipolar patients who were symptomatically stable on lithium.MethodNineteen subjects satisfying DSM–IV criteria for bipolar I disorder participated in a within-subject, double-blind, placebo-controlled random-order crossover study. Symptoms were evaluated following acute tryptophan depletion, which was induced by a 100 g amino acid drink following an overnight fast.ResultsPlasma tryptophan fell significantly after the depleting drink, but not after the control drink (P < 0.05, paired t-test, mean reduction 83%). No significant changes in mood or suicidality scores were recorded after acute tryptophan depletion.ConclusionsAcute tryptophan depletion does not reverse lithium's effects on mood and suicidality in bipolar disorder.


2004 ◽  
Vol 177 (1-2) ◽  
pp. 217-223 ◽  
Author(s):  
E. A. T. Evers ◽  
D. E. Tillie ◽  
F. M. van der Veen ◽  
C. K. Lieben ◽  
J. Jolles ◽  
...  

2004 ◽  
Vol 178 (1) ◽  
pp. 107-107
Author(s):  
E. A. T. Evers ◽  
D. E. Tillie ◽  
F. M. van der Veen ◽  
C. K. Lieben ◽  
J. Jolles ◽  
...  

2000 ◽  
Vol 176 (2) ◽  
pp. 182-188 ◽  
Author(s):  
H. E. J. Miller ◽  
J. F. W. Deakin ◽  
I. M. Anderson

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.


2011 ◽  
Vol 199 (5) ◽  
pp. 391-397 ◽  
Author(s):  
Sylvia M. L. Cox ◽  
Chawki Benkelfat ◽  
Alain Dagher ◽  
J. Scott Delaney ◽  
France Durand ◽  
...  

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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