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, Jahrgang 36, Nr. 10, 10.2015, S. 4031-40.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Transfer › Begutachtung
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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 -