Dissociable effects of noradrenaline, dopamine, and serotonin uptake blockade on stop task performance in rats
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RATIONALE: The stop-signal paradigm measures the ability to stop a motor response after its execution has been initiated. Impairments in inhibiting inappropriate behavior and prolonged stop-signal reaction times (SSRTs) are characteristic of several psychiatric disorders, most notably attention deficit/hyperactivity disorder. While there is relative consensus regarding the anatomical substrates of behavioral inhibition, the neurochemical imbalance responsible for the deficits in stopping displayed by impulsive individuals is still a matter of debate. OBJECTIVE: The aim of this study was to investigate the effects of manipulating brain monoamine levels on stop task parameters. METHODS: Lister-hooded rats were trained on the rodent version of the stop-signal task and administered different monoamine transporter inhibitors: citalopram, which selectively blocks the serotonin transporter; atomoxetine, which selectively blocks the noradrenaline transporter; and GBR-12909, which selectively blocks the dopamine transporter (DAT), and the alpha-2 adrenergic agonist guanfacine. RESULTS: Atomoxetine speeded SSRT and increased accuracy for go-trials. Citalopram slowed go reaction time and decreased go accuracy at the highest dose (1 mg/kg). GBR-12909 speeded go reaction time and impaired both go and stop accuracy. Guanfacine negatively modulated all principal stop and go measures at the highest dose used (0.3 mg/kg). CONCLUSIONS: The results suggest that atomoxetine exerts its beneficial effects on SSRT via its action on noradrenaline re-uptake, as the specific DAT blocker GBR-12909 and serotonin reuptake blockade had only minor effects on SSRT. The speeding of the go reaction time by dopamine reuptake blockade is consistent with the hypothesis that the hypothetical stop and go processes are modulated by distinct monoaminergic systems.
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Administration of methylphenidate and atomoxetine decreases SSRT in humans and animals, raising the possibility that noradrenalin is involved in motor response inhibition.
“Administration of methylphenidate and atomoxetine, which both target the dopamine and noradrenalin system, by inhibiting the re-uptake from the synaptic cleft, decreased SSRT in humans and in animals, raising the possibility that noradrenalin is involved in motor response inhibition as well (Chamberlain et al., 2006b; Eagle et al., 2007; Bari et al., 2009; Nandam et al., 2011).”
From Response Inhibition and Interference Control in Obsessive–Compulsive Spectrum Disorders (2014) · cites this paper as Bari et al., 2009
The Results (Experiment 2) report that atomoxetine decreased SSRT in rats, and the Discussion says this replicates findings in humans and suggests a role for noradrenaline in stopping. The paper does not test methylphenidate; its Discussion describes methylphenidate’s benefits as dependent on baseline conditions and notes a study in which it did not speed SSRT. The Introduction also describes atomoxetine as selective for the noradrenaline transporter, not as blocking both dopamine and noradrenaline reuptake. (LLM, conf=0.86)
Experimental — accuracy not yet measuredSerotonin does not seem to mediate performance of the Stop-signal task, as SSRIs and serotonin depletion did not affect action cancelation in humans or animals.
“Serotonin does not seem to mediate performance of the Stop-signal task, as use of selective serotonin re-uptake inhibitors (SSRIs) and serotonin depletion did not affect action cancelation in humans or in animals (Clark et al., 2005; Chamberlain et al., 2006b; Bari et al., 2009; Eagle et al., 2009; Drueke et al., 2010).”
From Response Inhibition and Interference Control in Obsessive–Compulsive Spectrum Disorders (2014) · cites this paper as Bari et al., 2009
Guanfacine reduces ascending norepinephrine release.
“Conversely, guanfacine, an agonist of α2-adrenergic autoreceptors, which reduces ascending norepinephrine release, worsens response inhibition in rats (Bari et al 2009, Bari et al 2011)”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Bari et al 2009
Guanfacine worsens response inhibition in rats.
“Conversely, guanfacine, an agonist of α2-adrenergic autoreceptors, which reduces ascending norepinephrine release, worsens response inhibition in rats (Bari et al 2009, Bari et al 2011)”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Bari et al 2009
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Stop signal reaction time deficits in a lifetime obsessive-compulsive disorder sample
McLaughlin, N. C. R., Kirschner, J., Foster, H., O’Connell, C., Rasmussen, S. A., & Greenberg, B. D. (2016) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617716000540 · Cited by 40 · see citing works
Kalanthroff, E., Teichert, T., Wheaton, M. G., Kimeldorf, M. B., Linkovski, O., Ahmari, S. E., Fyer, A. J., Schneier, F. R., Anholt, G. E., & Simpson, H. B. (2017) · Depression and Anxiety · doi:10.1002/da.22492 · Cited by 41 · see citing works
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- Authors
- Bari, A., Eagle, D. M., Mar, A. C., Robinson, E. S. J., & Robbins, T. W.
- Affiliations
- University of Cambridge (GB)
- University of Bristol (GB)
- Corresponding author
- Eagle, Dawn M.
- Venue
- Psychopharmacology
- Published
- 2009-04-30
- Volume
- 205
- Issue
- 2
- Pages
- 273-283
- ISSN
- 0033-3158 (ISSN-L)
- 1432-2072
- PMC
- PMC2705723
- OpenAlex
- W2130491227
- Cited by
- 194
- References
- 72
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 5 · 2023: 2 · 2022: 9 · 2021: 8 · 2020: 6 · 2019: 7 · 2018: 10 · 2017: 17 · 2016: 21 · 2015: 10 · 2014: 23 · 2013: 16 · 2012: 10
- FWCI
- 7.50
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Psychopharmacology (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Bristol Research (University of Bristol) (publishedVersion)
- Funders
- Pfizer
- Wellcome Trust (076274/Z/04/Z)
- British Pharmacological Society
- Research Councils UK
- University of Cambridge
- Medical Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Keywords
- stop-signal task, stop-signal reaction time, behavioral inhibition, monoamine transporters, norepinephrine uptake, dopamine reuptake, serotonin uptake, atomoxetine, citalopram, GBR 12909, guanfacine, attention deficit hyperactivity disorder, impulsivity
- MeSH terms
- Atomoxetine Hydrochloride, Analysis of Variance, Animals, Behavior, Animal, Conditioning, Operant, Dopamine, Dose-Response Relationship, Drug, Inhibition, Psychological, Male, Norepinephrine, Piperazines, Propylamines, Reaction Time, Serotonin, Task Performance and Analysis, Time Factors, Neurotransmitter Uptake Inhibitors, Citalopram, Guanfacine, Selective Serotonin Reuptake Inhibitors, Rats
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