Dissociable electrophysiological subprocesses during response inhibition are differentially modulated by dopamine D1 and D2 receptors

Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is known to play an important role. Many lines of psychophysiological research substantiate that two distinct response inhibition subprocesses ex...

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Published inEuropean neuropsychopharmacology Vol. 26; no. 6; pp. 1029 - 1036
Main Authors Beste, Christian, Stock, Ann-Kathrin, Epplen, Jörg T., Arning, Larissa
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.06.2016
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ISSN0924-977X
1873-7862
1873-7862
DOI10.1016/j.euroneuro.2016.03.002

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Abstract Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is known to play an important role. Many lines of psychophysiological research substantiate that two distinct response inhibition subprocesses exist, but it has remained elusive whether they can be attributed to distinct neurobiological factors governing the dopaminergic system. We, therefore, investigated this question by examining the effects of DRD1 (rs4532) and DRD2 (rs6277) receptor polymorphisms on electrophysiological correlates of response inhibition subprocesses (i.e., Nogo-N2 and Nogo-P3) in 195 healthy human subjects with a standard Go/Nogo task. The results show that response inhibition performance at a behavioral level is affected by DRD1 and DRD2 receptor variation. However, from an electrophysiological point of view these effects emerge via different mechanisms selectively affected by DRD1 and DRD2 receptor variation. While the D1 receptor system is associated with pre-motor inhibition electrophysiological correlates of response inhibition processes (Nogo-N2), the D2 receptor system is associated with electrophysiological correlates of outcome evaluation processes. Dissociable cognitive-neurophysiological subprocesses of response inhibition are hence attributable to distinct dopamine receptor systems.
AbstractList Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is known to play an important role. Many lines of psychophysiological research substantiate that two distinct response inhibition subprocesses exist, but it has remained elusive whether they can be attributed to distinct neurobiological factors governing the dopaminergic system. We, therefore, investigated this question by examining the effects of DRD1 (rs4532) and DRD2 (rs6277) receptor polymorphisms on electrophysiological correlates of response inhibition subprocesses (i.e., Nogo-N2 and Nogo-P3) in 195 healthy human subjects with a standard Go/Nogo task. The results show that response inhibition performance at a behavioral level is affected by DRD1 and DRD2 receptor variation. However, from an electrophysiological point of view these effects emerge via different mechanisms selectively affected by DRD1 and DRD2 receptor variation. While the D1 receptor system is associated with pre-motor inhibition electrophysiological correlates of response inhibition processes (Nogo-N2), the D2 receptor system is associated with electrophysiological correlates of outcome evaluation processes. Dissociable cognitive-neurophysiological subprocesses of response inhibition are hence attributable to distinct dopamine receptor systems.
Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is known to play an important role. Many lines of psychophysiological research substantiate that two distinct response inhibition subprocesses exist, but it has remained elusive whether they can be attributed to distinct neurobiological factors governing the dopaminergic system. We, therefore, investigated this question by examining the effects of DRD1 (rs4532) and DRD2 (rs6277) receptor polymorphisms on electrophysiological correlates of response inhibition subprocesses (i.e., Nogo-N2 and Nogo-P3) in 195 healthy human subjects with a standard Go/Nogo task. The results show that response inhibition performance at a behavioral level is affected by DRD1 and DRD2 receptor variation. However, from an electrophysiological point of view these effects emerge via different mechanisms selectively affected by DRD1 and DRD2 receptor variation. While the D1 receptor system is associated with pre-motor inhibition electrophysiological correlates of response inhibition processes (Nogo-N2), the D2 receptor system is associated with electrophysiological correlates of outcome evaluation processes. Dissociable cognitive-neurophysiological subprocesses of response inhibition are hence attributable to distinct dopamine receptor systems.
Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is known to play an important role. Many lines of psychophysiological research substantiate that two distinct response inhibition subprocesses exist, but it has remained elusive whether they can be attributed to distinct neurobiological factors governing the dopaminergic system. We, therefore, investigated this question by examining the effects of DRD1 (rs4532) and DRD2 (rs6277) receptor polymorphisms on electrophysiological correlates of response inhibition subprocesses (i.e., Nogo-N2 and Nogo-P3) in 195 healthy human subjects with a standard Go/Nogo task. The results show that response inhibition performance at a behavioral level is affected by DRD1 and DRD2 receptor variation. However, from an electrophysiological point of view these effects emerge via different mechanisms selectively affected by DRD1 and DRD2 receptor variation. While the D1 receptor system is associated with pre-motor inhibition electrophysiological correlates of response inhibition processes (Nogo-N2), the D2 receptor system is associated with electrophysiological correlates of outcome evaluation processes. Dissociable cognitive-neurophysiological subprocesses of response inhibition are hence attributable to distinct dopamine receptor systems.Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is known to play an important role. Many lines of psychophysiological research substantiate that two distinct response inhibition subprocesses exist, but it has remained elusive whether they can be attributed to distinct neurobiological factors governing the dopaminergic system. We, therefore, investigated this question by examining the effects of DRD1 (rs4532) and DRD2 (rs6277) receptor polymorphisms on electrophysiological correlates of response inhibition subprocesses (i.e., Nogo-N2 and Nogo-P3) in 195 healthy human subjects with a standard Go/Nogo task. The results show that response inhibition performance at a behavioral level is affected by DRD1 and DRD2 receptor variation. However, from an electrophysiological point of view these effects emerge via different mechanisms selectively affected by DRD1 and DRD2 receptor variation. While the D1 receptor system is associated with pre-motor inhibition electrophysiological correlates of response inhibition processes (Nogo-N2), the D2 receptor system is associated with electrophysiological correlates of outcome evaluation processes. Dissociable cognitive-neurophysiological subprocesses of response inhibition are hence attributable to distinct dopamine receptor systems.
Abstract Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is known to play an important role. Many lines of psychophysiological research substantiate that two distinct response inhibition subprocesses exist, but it has remained elusive whether they can be attributed to distinct neurobiological factors governing the dopaminergic system. We, therefore, investigated this question by examining the effects of DRD1 (rs4532) and DRD2 (rs6277) receptor polymorphisms on electrophysiological correlates of response inhibition subprocesses (i.e., Nogo-N2 and Nogo-P3) in 195 healthy human subjects with a standard Go/Nogo task. The results show that response inhibition performance at a behavioral level is affected by DRD1 and DRD2 receptor variation. However, from an electrophysiological point of view these effects emerge via different mechanisms selectively affected by DRD1 and DRD2 receptor variation. While the D1 receptor system is associated with pre-motor inhibition electrophysiological correlates of response inhibition processes (Nogo-N2), the D2 receptor system is associated with electrophysiological correlates of outcome evaluation processes. Dissociable cognitive-neurophysiological subprocesses of response inhibition are hence attributable to distinct dopamine receptor systems.
Author Epplen, Jörg T.
Arning, Larissa
Stock, Ann-Kathrin
Beste, Christian
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  fullname: Arning, Larissa
  organization: Department of Human Genetics, Medical Faculty, Ruhr-Universität Bochum, Germany
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Keywords Response inhibition
Dopamine
DRD1
DRD2
EEG
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Snippet Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic systems is...
Abstract Action control is achieved through a multitude of cognitive processes. One of them is the ability to inhibit responses, for which the dopaminergic...
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SubjectTerms Adolescent
Adult
Dopamine
DRD1
DRD2
EEG
Electroencephalography
Electrophysiological Phenomena - genetics
Female
Genotype
Humans
Inhibition (Psychology)
Internal Medicine
Male
Polymorphism, Genetic - genetics
Psychiatry
Psychomotor Performance
Receptors, Dopamine D1 - genetics
Receptors, Dopamine D2 - genetics
Response inhibition
Young Adult
Title Dissociable electrophysiological subprocesses during response inhibition are differentially modulated by dopamine D1 and D2 receptors
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https://dx.doi.org/10.1016/j.euroneuro.2016.03.002
https://www.ncbi.nlm.nih.gov/pubmed/27021648
https://www.proquest.com/docview/1795868164
https://www.proquest.com/docview/1808707248
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