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Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder

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Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder. / Zhukovsky, Peter; Morein-Zamir, Sharon; Ziauddeen, Hisham; Fernandez-Egea, Emilio; Meng, Chun; Regenthal, Ralf; Sahakian, Barbara J; Bullmore, Edward T; Robbins, Trevor W; Dalley, Jeffrey W; Ersche, Karen D.

In: BIOL PSYCHIAT-COGN N, Vol. 7, No. 11, 11.2022, p. 1116-1126.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Zhukovsky, P, Morein-Zamir, S, Ziauddeen, H, Fernandez-Egea, E, Meng, C, Regenthal, R, Sahakian, BJ, Bullmore, ET, Robbins, TW, Dalley, JW & Ersche, KD 2022, 'Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder', BIOL PSYCHIAT-COGN N, vol. 7, no. 11, pp. 1116-1126. https://doi.org/10.1016/j.bpsc.2021.08.010

APA

Zhukovsky, P., Morein-Zamir, S., Ziauddeen, H., Fernandez-Egea, E., Meng, C., Regenthal, R., Sahakian, B. J., Bullmore, E. T., Robbins, T. W., Dalley, J. W., & Ersche, K. D. (2022). Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder. BIOL PSYCHIAT-COGN N, 7(11), 1116-1126. https://doi.org/10.1016/j.bpsc.2021.08.010

Vancouver

Zhukovsky P, Morein-Zamir S, Ziauddeen H, Fernandez-Egea E, Meng C, Regenthal R et al. Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder. BIOL PSYCHIAT-COGN N. 2022 Nov;7(11):1116-1126. https://doi.org/10.1016/j.bpsc.2021.08.010

Bibtex

@article{9d8d7c2ab81a4a4189791491fd0a3e63,
title = "Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder",
abstract = "BACKGROUND: Impaired response inhibition in individuals with cocaine use disorder (CUD) is hypothesized to depend on deficient noradrenergic signaling in corticostriatal networks. Remediation of noradrenergic neurotransmission with selective norepinephrine reuptake inhibitors such as atomoxetine may therefore have clinical utility to improve response inhibitory control in CUD.METHODS: We carried out a randomized, double-blind, placebo-controlled, crossover study with 26 participants with CUD and 28 control volunteers investigating the neural substrates of stop-signal inhibitory control. The effects of a single dose of atomoxetine (40 mg) were compared with placebo on stop-signal reaction time performance and functional network connectivity using dynamic causal modeling.RESULTS: We found that atomoxetine speeded Go response times in both control participants and those with CUD. Improvements in stopping efficiency on atomoxetine were conditional on baseline (placebo) stopping performance and were directly associated with increased inferior frontal gyrus activation. Further, stopping performance, task-based brain activation, and effective connectivity were similar in the 2 groups. Dynamic causal modeling of effective connectivity of multiple prefrontal and basal ganglia regions replicated and extended previous models of network function underlying inhibitory control to CUD and control volunteers and showed subtle effects of atomoxetine on prefrontal-basal ganglia interactions.CONCLUSIONS: These findings demonstrate that atomoxetine improves response inhibition in a baseline-dependent manner in control participants and in those with CUD. Our results emphasize inferior frontal cortex function as a future treatment target owing to its key role in improving response inhibition in CUD.",
author = "Peter Zhukovsky and Sharon Morein-Zamir and Hisham Ziauddeen and Emilio Fernandez-Egea and Chun Meng and Ralf Regenthal and Sahakian, {Barbara J} and Bullmore, {Edward T} and Robbins, {Trevor W} and Dalley, {Jeffrey W} and Ersche, {Karen D}",
note = "Copyright {\textcopyright} 2021 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.",
year = "2022",
month = nov,
doi = "10.1016/j.bpsc.2021.08.010",
language = "English",
volume = "7",
pages = "1116--1126",
journal = "BIOL PSYCHIAT-COGN N",
issn = "2451-9022",
publisher = "Elsevier Inc.",
number = "11",

}

RIS

TY - JOUR

T1 - Prefrontal Cortex Activation and Stopping Performance Underlie the Beneficial Effects of Atomoxetine on Response Inhibition in Healthy Volunteers and Those With Cocaine Use Disorder

AU - Zhukovsky, Peter

AU - Morein-Zamir, Sharon

AU - Ziauddeen, Hisham

AU - Fernandez-Egea, Emilio

AU - Meng, Chun

AU - Regenthal, Ralf

AU - Sahakian, Barbara J

AU - Bullmore, Edward T

AU - Robbins, Trevor W

AU - Dalley, Jeffrey W

AU - Ersche, Karen D

N1 - Copyright © 2021 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

PY - 2022/11

Y1 - 2022/11

N2 - BACKGROUND: Impaired response inhibition in individuals with cocaine use disorder (CUD) is hypothesized to depend on deficient noradrenergic signaling in corticostriatal networks. Remediation of noradrenergic neurotransmission with selective norepinephrine reuptake inhibitors such as atomoxetine may therefore have clinical utility to improve response inhibitory control in CUD.METHODS: We carried out a randomized, double-blind, placebo-controlled, crossover study with 26 participants with CUD and 28 control volunteers investigating the neural substrates of stop-signal inhibitory control. The effects of a single dose of atomoxetine (40 mg) were compared with placebo on stop-signal reaction time performance and functional network connectivity using dynamic causal modeling.RESULTS: We found that atomoxetine speeded Go response times in both control participants and those with CUD. Improvements in stopping efficiency on atomoxetine were conditional on baseline (placebo) stopping performance and were directly associated with increased inferior frontal gyrus activation. Further, stopping performance, task-based brain activation, and effective connectivity were similar in the 2 groups. Dynamic causal modeling of effective connectivity of multiple prefrontal and basal ganglia regions replicated and extended previous models of network function underlying inhibitory control to CUD and control volunteers and showed subtle effects of atomoxetine on prefrontal-basal ganglia interactions.CONCLUSIONS: These findings demonstrate that atomoxetine improves response inhibition in a baseline-dependent manner in control participants and in those with CUD. Our results emphasize inferior frontal cortex function as a future treatment target owing to its key role in improving response inhibition in CUD.

AB - BACKGROUND: Impaired response inhibition in individuals with cocaine use disorder (CUD) is hypothesized to depend on deficient noradrenergic signaling in corticostriatal networks. Remediation of noradrenergic neurotransmission with selective norepinephrine reuptake inhibitors such as atomoxetine may therefore have clinical utility to improve response inhibitory control in CUD.METHODS: We carried out a randomized, double-blind, placebo-controlled, crossover study with 26 participants with CUD and 28 control volunteers investigating the neural substrates of stop-signal inhibitory control. The effects of a single dose of atomoxetine (40 mg) were compared with placebo on stop-signal reaction time performance and functional network connectivity using dynamic causal modeling.RESULTS: We found that atomoxetine speeded Go response times in both control participants and those with CUD. Improvements in stopping efficiency on atomoxetine were conditional on baseline (placebo) stopping performance and were directly associated with increased inferior frontal gyrus activation. Further, stopping performance, task-based brain activation, and effective connectivity were similar in the 2 groups. Dynamic causal modeling of effective connectivity of multiple prefrontal and basal ganglia regions replicated and extended previous models of network function underlying inhibitory control to CUD and control volunteers and showed subtle effects of atomoxetine on prefrontal-basal ganglia interactions.CONCLUSIONS: These findings demonstrate that atomoxetine improves response inhibition in a baseline-dependent manner in control participants and in those with CUD. Our results emphasize inferior frontal cortex function as a future treatment target owing to its key role in improving response inhibition in CUD.

U2 - 10.1016/j.bpsc.2021.08.010

DO - 10.1016/j.bpsc.2021.08.010

M3 - SCORING: Journal article

C2 - 34508901

VL - 7

SP - 1116

EP - 1126

JO - BIOL PSYCHIAT-COGN N

JF - BIOL PSYCHIAT-COGN N

SN - 2451-9022

IS - 11

ER -