Inhibitory Control in Rats Performing a Stop-Signal Reaction-Time Task: Effects of Lesions of the Medial Striatum and d-Amphetamine.
Abstract
The stop-signal task measures the ability to inhibit a response that has already been initiated, that is, the ability to stop. Imaging studies have implicated frontostriatal circuitry in the mediation of this form of response control. The authors report inhibition functions of normal rats and those with medial striatal damage performing the stop-signal task. Excitotoxic lesions of the medial striatum produced significant deficits on task performance, including increased omissions on the go task and flattened inhibition function, possibly as a result of increased reaction-time mean and variability. Medial striatal lesions also significantly slowed stop-signal reaction time. Subsequent treatment with d-amphetamine removed (0.3 mg/kg) or exacerbated (1.0 mg/kg) this deficit.
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OFC and infralimbic mPFC mediate response inhibition, as lesions produce premature responding in the 5-CSRTT and SSRT.
“OFC and infralimbic (IL) mPFC have been shown to mediate response inhibition, as lesions of these areas produce premature responding in the 5-CSRTT and SSRT (Chudasama et al 2003, Eagle et al 2008a, Eagle & Robbins 2003).”
From Prefrontal cortex executive processes affected by stress in health and disease (2018) · cites this paper as Eagle & Robbins 2003
Lesion studies suggest that lesions of the medial striatum in rodents lead to overall longer stop signal reaction time.
“Lesion studies also suggest that lesions of the medial striatum in rodents lead to overall longer stop signal reaction time (Eagle and Robbins 2003).”
From Large-scale functional neural network correlates of response inhibition: an fMRI meta-analysis (2017) · cites this paper as Eagle and Robbins 2003
Basal ganglia lesions impaired stop performance in humans and rodents, while deep-brain stimulation of STN in Parkinson patients improved inhibitory control.
“Lesions to the basal ganglia impaired stop performance for both humans and rodents [26–28], whereas deep-brain stimulation of STN in Parkinson patients enhanced inhibitory control [29].”
From Response inhibition in the stop-signal paradigm (2008) · cites this paper as [28]
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- Authors
- Eagle, D. M., & Robbins, T. W.
- Affiliations
- University of Cambridge (GB)
- Venue
- Behavioral Neuroscience
- Published
- 2003-12
- Volume
- 117
- Issue
- 6
- Pages
- 1302-1317
- ISSN
- 0735-7044 (ISSN-L)
- 1939-0084
- OpenAlex
- W1991271750
- Cited by
- 252
- References
- 67
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 8 · 2023: 4 · 2022: 6 · 2021: 9 · 2020: 11 · 2019: 7 · 2018: 7 · 2017: 15 · 2016: 17 · 2015: 12 · 2014: 16 · 2013: 22 · 2012: 18
- FWCI
- 2.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Behavioral Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Neural and Behavioral Psychology Studies
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- inhibitory control, stop-signal task, medial striatum, excitotoxic lesions, d-amphetamine, frontostriatal circuits, response inhibition, reaction time
- MeSH terms
- Central Nervous System Stimulants, Animals, Corpus Striatum, Dextroamphetamine, Inhibition, Psychological, Male, Motor Activity, Psychomotor Performance, Reaction Time, Rats
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