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Prefrontal and Monoaminergic Contributions to Stop-Signal Task Performance in Rats
Open accessAbstract
Defining the neural and neurochemical substrates of response inhibition is of crucial importance for the study and treatment of pathologies characterized by impulsivity such as attention-deficit/hyperactivity disorder and addiction. The stop-signal task (SST) is one of the most popular paradigms used to study the speed and efficacy of inhibitory processes in humans and other animals. Here we investigated the effect of temporarily inactivating different prefrontal subregions in the rat by means of muscimol microinfusions on SST performance. We found that dorsomedial prefrontal cortical areas are important for inhibiting an already initiated response. We also investigated the possible neural substrates of the selective noradrenaline reuptake inhibitor atomoxetine via its local microinfusion into different subregions of the rat prefrontal cortex. Our results show that both orbitofrontal and dorsal prelimbic cortices mediate the beneficial effects of atomoxetine on SST performance. To assess the neurochemical specificity of these effects, we infused the α2-adrenergic agonist guanfacine and the D(1)/D(2) antagonist α-flupenthixol in dorsal prelimbic cortex to interfere with noradrenergic and dopaminergic neurotransmission, respectively. Guanfacine, which modulates noradrenergic neurotransmission, selectively impaired stopping, whereas blocking dopaminergic receptors by α-flupenthixol infusion prolonged go reaction time only, confirming the important role of noradrenergic neurotransmission in response inhibition. These results show that, similar to humans, distinct networks play important roles during SST performance in the rat and that they are differentially modulated by noradrenergic and dopaminergic neurotransmission. This study advances our understanding of the neuroanatomical and neurochemical determinants of impulsivity, which are relevant for a range of psychiatric disorders.
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“blocking either D1 or D2 in the mPFC or OFC had no effect on the 5-CRSTT (Granon et al 2000, Winstanley et al 2010), or the SST (Bari et al 2011, Bari & Robbins 2013b)”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Bari et al 2011
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“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 2011
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“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 2011
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Metadata
- Authors
- Bari, A., Mar, A. C., Theobald, D. E., Elands, S. A., Oganya, K. C. N. A., Eagle, D. M., & Robbins, T. W.
- Affiliations
- University of Cambridge (GB)
- Corresponding author
- Bari, A.
- Venue
- Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2011-06-22
- Volume
- 31
- Issue
- 25
- Pages
- 9254-9263
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC3145112
- OpenAlex
- W2056110254
- Cited by
- 188
- References
- 100
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 29 · 2023: 8 · 2022: 8 · 2021: 16 · 2020: 8 · 2019: 6 · 2018: 5 · 2017: 16 · 2016: 14 · 2015: 19 · 2014: 20 · 2013: 20 · 2012: 13
- FWCI
- 8.60
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Eli Lilly and Company
- Wellcome Trust (089589/Z/09/Z, 089589, 093875)
- University of Cambridge
- Medical Research Council (G0001354, 089589/Z/09/Z)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Keywords
- stop-signal task, response inhibition, prefrontal cortex, dorsomedial prefrontal cortex, orbitofrontal cortex, norepinephrine, dopamine, atomoxetine, guanfacine, alpha-flupenthixol, impulsivity, attention deficit hyperactivity disorder, addiction, muscimol inactivation, rats
- MeSH terms
- Animals, Impulsive Behavior, Male, Neural Inhibition, Psychomotor Performance, Biogenic Monoamines, Prefrontal Cortex, Rats
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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