Cited by 188Neural and Behavioral Psychology StudiesNeurotransmitter Receptor Influence on BehaviorAttention Deficit Hyperactivity Disorder

Prefrontal and monoaminergic contributions to stop-signal task performance in rats

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Bari, A., Mar, A. C., Theobald, D. E., Elands, S. A., Oganya, K. C. N. A., Eagle, D. M., Robbins, T. W.·2011·Journal of Neuroscience

Abstract

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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Crossref · 10.1523/jneurosci.1543-11.2011

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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
Published
2011-06-22
Volume
31
Issue
25
Pages
9254-9263
ISSN
  • 0270-6474 (ISSN-L)
  • 1529-2401
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
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

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