Interactions between glutamate, dopamine, and the neuronal signature of response inhibition in the human striatum

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Interactions between glutamate, dopamine, and the neuronal signature of response inhibition in the human striatum. / Lorenz, Robert; Gleich, Tobias; Buchert, Ralph; Schlagenhauf, Florian; Kühn, Simone; Gallinat, Jürgen.

In: HUM BRAIN MAPP, Vol. 36, No. 10, 10.2015, p. 4031-40.

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@article{ef64a048b0c74304935245e4d95951f6,
title = "Interactions between glutamate, dopamine, and the neuronal signature of response inhibition in the human striatum",
abstract = "Response inhibition is a basic mechanism in cognitive control and dysfunctional in major psychiatric disorders. The neuronal mechanisms are in part driven by dopamine in the striatum. Animal data suggest a regulatory role of glutamate on the level of the striatum. We used a trimodal imaging procedure of the human striatum including F18-DOPA positron emission tomography, proton magnetic resonance spectroscopy, and functional magnetic resonance imaging of a stop signal task. We investigated dopamine synthesis capacity and glutamate concentration in vivo and their relation to functional properties of response inhibition. A mediation analysis revealed a significant positive association between dopamine synthesis capacity and inhibition-related neural activity in the caudate nucleus. This relationship was significantly mediated by striatal glutamate concentration. Furthermore, stop signal reaction time was inversely related to striatal activity during inhibition. The data show, for the first time in humans, an interaction between dopamine, glutamate, and the neural signature of response inhibition in the striatum. This finding stresses the importance of the dopamine-glutamate interaction for behavior and may facilitate the understanding of psychiatric disorders characterized by impaired response inhibition.",
keywords = "Adult, Aging/physiology, Brain Mapping, Caudate Nucleus/cytology, Corpus Striatum/cytology, Dopamine/physiology, Dopaminergic Neurons/diagnostic imaging, Female, Glutamic Acid/physiology, Humans, Inhibition, Psychological, Magnetic Resonance Imaging, Male, Neurons/diagnostic imaging, Positron-Emission Tomography, Psychomotor Performance/physiology, Reaction Time/physiology",
author = "Robert Lorenz and Tobias Gleich and Ralph Buchert and Florian Schlagenhauf and Simone K{\"u}hn and J{\"u}rgen Gallinat",
note = "{\textcopyright} 2015 Wiley Periodicals, Inc.",
year = "2015",
month = oct,
doi = "10.1002/hbm.22895",
language = "English",
volume = "36",
pages = "4031--40",
journal = "HUM BRAIN MAPP",
issn = "1065-9471",
publisher = "Wiley-Liss Inc.",
number = "10",

}

RIS

TY - JOUR

T1 - Interactions between glutamate, dopamine, and the neuronal signature of response inhibition in the human striatum

AU - Lorenz, Robert

AU - Gleich, Tobias

AU - Buchert, Ralph

AU - Schlagenhauf, Florian

AU - Kühn, Simone

AU - Gallinat, Jürgen

N1 - © 2015 Wiley Periodicals, Inc.

PY - 2015/10

Y1 - 2015/10

N2 - Response inhibition is a basic mechanism in cognitive control and dysfunctional in major psychiatric disorders. The neuronal mechanisms are in part driven by dopamine in the striatum. Animal data suggest a regulatory role of glutamate on the level of the striatum. We used a trimodal imaging procedure of the human striatum including F18-DOPA positron emission tomography, proton magnetic resonance spectroscopy, and functional magnetic resonance imaging of a stop signal task. We investigated dopamine synthesis capacity and glutamate concentration in vivo and their relation to functional properties of response inhibition. A mediation analysis revealed a significant positive association between dopamine synthesis capacity and inhibition-related neural activity in the caudate nucleus. This relationship was significantly mediated by striatal glutamate concentration. Furthermore, stop signal reaction time was inversely related to striatal activity during inhibition. The data show, for the first time in humans, an interaction between dopamine, glutamate, and the neural signature of response inhibition in the striatum. This finding stresses the importance of the dopamine-glutamate interaction for behavior and may facilitate the understanding of psychiatric disorders characterized by impaired response inhibition.

AB - Response inhibition is a basic mechanism in cognitive control and dysfunctional in major psychiatric disorders. The neuronal mechanisms are in part driven by dopamine in the striatum. Animal data suggest a regulatory role of glutamate on the level of the striatum. We used a trimodal imaging procedure of the human striatum including F18-DOPA positron emission tomography, proton magnetic resonance spectroscopy, and functional magnetic resonance imaging of a stop signal task. We investigated dopamine synthesis capacity and glutamate concentration in vivo and their relation to functional properties of response inhibition. A mediation analysis revealed a significant positive association between dopamine synthesis capacity and inhibition-related neural activity in the caudate nucleus. This relationship was significantly mediated by striatal glutamate concentration. Furthermore, stop signal reaction time was inversely related to striatal activity during inhibition. The data show, for the first time in humans, an interaction between dopamine, glutamate, and the neural signature of response inhibition in the striatum. This finding stresses the importance of the dopamine-glutamate interaction for behavior and may facilitate the understanding of psychiatric disorders characterized by impaired response inhibition.

KW - Adult

KW - Aging/physiology

KW - Brain Mapping

KW - Caudate Nucleus/cytology

KW - Corpus Striatum/cytology

KW - Dopamine/physiology

KW - Dopaminergic Neurons/diagnostic imaging

KW - Female

KW - Glutamic Acid/physiology

KW - Humans

KW - Inhibition, Psychological

KW - Magnetic Resonance Imaging

KW - Male

KW - Neurons/diagnostic imaging

KW - Positron-Emission Tomography

KW - Psychomotor Performance/physiology

KW - Reaction Time/physiology

U2 - 10.1002/hbm.22895

DO - 10.1002/hbm.22895

M3 - SCORING: Journal article

C2 - 26177932

VL - 36

SP - 4031

EP - 4040

JO - HUM BRAIN MAPP

JF - HUM BRAIN MAPP

SN - 1065-9471

IS - 10

ER -