Functional Dissociation in Right Inferior Frontal Cortex during Performance of Go/No-Go Task

Chikazoe, Junichi; Jimura, Koji; Asari, Tomoki; Yamashita, Ken; Morimoto, Hiroki M.; Hirose, Satoshi; Miyashita, Yasushi; Konishi, Seiki

doi:10.1093/cercor/bhn065

Cited by 250 publications

(278 citation statements)

References 55 publications

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“…confounding inhibitory demands with attentional capture because of low no-go stimulus frequency (Chikazoe et al, 2009a;Criaud and Boulinguez, 2013). Interestingly, the contrast correct no-go4incorrect no-go showed no significant pharmacogenetic effect at the chosen level of statistical significance.…”

Section: Pharmacogenetic Findingsmentioning

confidence: 88%

“…Using the most stringent contrast to isolate inhibitory mechanisms in the Go/No-Go task (correct no-go4correct odd) (Chikazoe et al, 2009a), we found an interaction between SLC6A3 genotype and drug condition for BOLD during successful inhibition. The interaction indicated a BOLD increase with MPH in 9R carriers, but a decrease in 10/10 homozygotes.…”

Section: Pharmacogenetic Findingsmentioning

confidence: 91%

“…In contrast, the direct comparison of successful with failed no-go trials in the contrast correct no-go4 incorrect no-go does not isolate this task demand factor but most likely identifies differences due to success in inhibition and the commitment and processing of an error. Therefore, it may be concluded that our pharmacogenetic effects, despite our attempt to use a cognitively specific contrast to isolate response inhibition (Chikazoe et al, 2009a), may be due in part to general factors such as task demand.…”

Section: Pharmacogenetic Findingsmentioning

confidence: 96%

“…The event-related Go/No-Go task (Chikazoe et al, 2009a) involved 200 go trials, 30 oddball trials, and 30 no-go trials. Each trial consisted of a colored circle presented for 500 ms on black background in the middle of the screen, followed by 1300 ms (jittered 1100-1500 ms) of black background.…”

Section: Go/no-go Task and Analysismentioning

confidence: 99%

“…The conditions (1) correct no-go trials, (2) incorrect no-go trials, (3) correct oddball trials, (4) incorrect oddball trials, and (5) incorrect go trials were modeled using a synthetic canonical hemodynamic response function. Go trials served as baseline (Chamberlain et al, 2009;Chikazoe et al, 2009a). Individual realignment parameters were included as multiple regressors.…”

Section: Go/no-go Task and Analysismentioning

confidence: 99%

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Methylphenidate Effects on Brain Activity as a Function of SLC6A3 Genotype and Striatal Dopamine Transporter Availability

Kasparbauer

Rujescu²,

Riedel

et al. 2014

Neuropsychopharmacol

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We pharmacologically challenged catecholamine reuptake, using methylphenidate, to investigate its effects on brain activity during a motor response inhibition task as a function of the 3 0 -UTR variable number of tandem repeats (VNTR) polymorphism of the dopamine transporter (DAT) gene (SLC6A3) and the availability of DATs in the striatum. We measured the cerebral hemodynamic response of 50 healthy males during a Go/No-Go task, a measure of cognitive control, under the influence of 40 mg methylphenidate and placebo using 3T functional magnetic resonance imaging. Subjects were grouped into 9-repeat (9R) carriers and 10/10 homozygotes on the basis of the SLC6A3 VNTR. During successful no-go trials compared with oddball trials, methylphenidate induced an increase of blood oxygen level-dependent (BOLD) signal for carriers of the SLC6A3 9R allele but a decrease in 10/10 homozygotes in a thalamocortical network. The same pattern was observed in caudate and inferior frontal gyrus when successful no-go trials were compared with successful go trials. We additionally investigated in a subset of 35 participants whether baseline striatal DAT availability, ascertained with 123 I-FP-CIT single photon emission computed tomography, predicted the amount of methylphenidate-induced change in hemodynamic response or behavior. Striatal DAT availability was nominally greater in 9R carriers compared with 10/10 homozygotes (d ¼ 0.40), in line with metaanalyses, but did not predict BOLD or behavioral changes following MPH administration. We conclude that the effects of acute MPH administration on brain activation are dependent on DAT genotype, with 9R carriers showing enhanced BOLD following administration of a prodopaminergic compound.

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Section: Pharmacogenetic Findingsmentioning

confidence: 88%

Section: Pharmacogenetic Findingsmentioning

confidence: 91%

Section: Pharmacogenetic Findingsmentioning

confidence: 96%

Section: Go/no-go Task and Analysismentioning

confidence: 99%

Section: Go/no-go Task and Analysismentioning

confidence: 99%

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Methylphenidate Effects on Brain Activity as a Function of SLC6A3 Genotype and Striatal Dopamine Transporter Availability

Kasparbauer

Rujescu²,

Riedel

et al. 2014

Neuropsychopharmacol

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Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability

et al. 2017

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IMPORTANCE Tobacco use disorder is associated with dysregulated neurocognitive function in the right inferior frontal gyrus (IFG)—one node in a corticothalamic inhibitory control (IC) network. OBJECTIVE To examine associations between IC neural circuitry structure and function and lapse/relapse vulnerability in 2 independent studies of adult smokers. DESIGN, SETTING, AND PARTICIPANTS In study 1, treatment-seeking smokers (n = 81) completed an IC task during functional magnetic resonance imaging (fMRI) before making a quit attempt and then were followed up for 10 weeks after their quit date. In study 2, a separate group of smokers (n = 26) performed the same IC task during fMRI, followed by completing a laboratory-based smoking relapse analog task. Study 1 was performed at Duke University Medical Center between 2008 and 2012; study 2 was conducted at the Medical University of South Carolina between 2013 and 2016. MAIN OUTCOMES AND MEASURES Associations between corticothalamic-mediated IC, gray-matter volume, and smoking lapse/relapse. RESULTS Of the 81 study participants in study 1 (cessation study), 45 were women (56%), with mean (SD) age, 38.4 (10.2) years. In study 1, smoking relapse was associated with less gray-matter volume (F1,74 = 28.32; familywise error P threshold = 0.03), greater IC task-related blood oxygenation level–dependent (BOLD) response in the right IFG (F1,78 = 14.87) and thalamus (F1,78 = 14.97) (P < .05), and weaker corticothalamic task-based functional connectivity (tbFC) (F1,77 = 5.87; P = .02). Of the 26 participants in study 2 (laboratory study), 15 were women (58%), with mean (SD) age, 34.9 (10.3). Similar to study 1, in study 2, greater IC-BOLD response in the right IFG (t23 = −2.49; β = −0.47; P = .02), and weaker corticothalamic tbFC (t22 = 5.62; β = 0.79; P < .001) were associated with smoking sooner during the smoking relapse-analog task. In both studies, corticothalamic tbFC mediated the association between IC performance and smoking outcomes. CONCLUSIONS AND RELEVANCE In these 2 studies, baseline differences in corticothalamic circuitry function were associated with mediated IC and smoking relapse vulnerability. These findings warrant further examination of interventions for augmenting corticothalamic neurotransmission and enhancing IC during the course of tobacco use disorder treatment.

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The functional anatomy of cognitive control: A domain‐general brain network for uncertainty processing

Chen

Spagna

et al. 2019

J of Comparative Neurology

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Cognitive control is the coordination of mental operations under conditions of uncertainty in accordance with goal‐directed behaviors, and plays a key role in the domains of executive control, working memory, and decision‐making. Although there is emerging evidence of common involvement of the cognitive control network (CCN) of the brain in these domains, this network has mostly been linked to the processing of conflict, which is just one case of an increase in uncertainty. Here, we conducted an activation‐likelihood‐estimation‐based large‐scale meta‐analysis of 289 functional magnetic resonance imaging studies in the three domains to examine the common involvement of the CCN in uncertainty processing by contrasting the high‐uncertainty versus low‐uncertainty conditions. We found a general association between increase in uncertainty and an activation increase in regions of the CCN, including the frontoparietal network (comprising the frontal eye fields, the areas near and along the intraparietal sulcus, and the dorsolateral prefrontal cortex), the cingulo‐opercular network (including the anterior cingulate cortex extending to the supplementary motor area, and the anterior insular cortex), and a subcortical structure (the striatum). These results demonstrate that the CCN is a domain‐general construct underlying uncertainty processing to support goal‐directed behaviors.

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Functional Dissociation in Right Inferior Frontal Cortex during Performance of Go/No-Go Task

Cited by 250 publications

References 55 publications

Methylphenidate Effects on Brain Activity as a Function of SLC6A3 Genotype and Striatal Dopamine Transporter Availability

Methylphenidate Effects on Brain Activity as a Function of SLC6A3 Genotype and Striatal Dopamine Transporter Availability

Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability

The functional anatomy of cognitive control: A domain‐general brain network for uncertainty processing

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