Contrasting roles for dopamine D1 and D2 receptor subtypes in the dorsomedial striatum but not the nucleus accumbens core during behavioral inhibition in the stop-signal task in rats

Dopamine and dopamine-receptor function are often implicated in behavioral inhibition, and deficiencies within behavioral inhibition processes linked to attention deficit/hyperactivity disorder (ADHD), schizophrenia, obsessive-compulsive disorder, and drug addiction. In the stop-signal task, which m...

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Published inThe Journal of neuroscience Vol. 31; no. 20; pp. 7349 - 7356
Main Authors Eagle, Dawn M, Wong, Jacky C K, Allan, Michelle E, Mar, Adam C, Theobald, David E, Robbins, Trevor W
Format Journal Article
LanguageEnglish
Published United States Society for Neuroscience 18.05.2011
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Summary:Dopamine and dopamine-receptor function are often implicated in behavioral inhibition, and deficiencies within behavioral inhibition processes linked to attention deficit/hyperactivity disorder (ADHD), schizophrenia, obsessive-compulsive disorder, and drug addiction. In the stop-signal task, which measures the speed of the process of inhibition [stop-signal reaction time (SSRT)], psychostimulant-related improvement of SSRT in ADHD is linked with dopamine function. However, the precise nature of dopaminergic control over SSRT remains unclear. This study examined region- and receptor-specific modulation of SSRT in the rat using direct infusions of the dopamine D1 receptor (DRD1) antagonist SCH 23390 or dopamine D2 receptor (DRD2) antagonist sulpiride into the dorsomedial striatum (DMStr) or nucleus accumbens core (NAcbC). DRD1 and DRD2 antagonists had contrasting effects on SSRT that were specific to the DMStr. SCH 23390 decreased SSRT with little effect on the go response. Conversely, sulpiride increased SSRT but also increased go-trial reaction time and reduced trial completion at the highest doses. These results suggest that DRD1 and DRD2 function within the DMStr, but not the NAcbC, may act to balance behavioral inhibition in a manner that is independent of behavioral activation.
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Author contributions: D.M.E. and T.W.R. designed research; D.M.E., J.C.W., and M.E.A. performed research; A.C.M. and D.T. contributed unpublished reagents/analytic tools; D.M.E. analyzed data; D.M.E. wrote the paper.
ISSN:0270-6474
1529-2401
1529-2401
DOI:10.1523/JNEUROSCI.6182-10.2011