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

Association Between Baseline Corticothalamic-Mediated Inhibitory Control and Smoking Relapse Vulnerability.
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DOI:
10.1001/jamapsychiatry.2017.0017
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发表时间:
2017-04-01
期刊:
影响因子:
25.8
通讯作者:
McClernon FJ
McClernon FJ
中科院分区:
医学1区
文献类型:
--
作者:
Froeliger B;McConnell PA;Bell S;Sweitzer M;Kozink RV;Eichberg C;Hallyburton M;Kaiser N;Gray KM;McClernon FJ

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烟草使用障碍与右侧额下回(IFG)的神经认知功能失调有关,IFG是皮质丘脑抑制控制(IC)网络中的一个节点。在2项独立的成年吸烟者研究中,研究IC神经回路结构和功能与失效/复发易感性之间的关系。在研究1中,寻求治疗的吸烟者(n = 81)在尝试戒烟前完成了功能磁共振成像(fMRI)期间的IC任务,然后在戒烟日期后随访10周。在研究2中,另一组吸烟者(n = 26)在fMRI期间执行相同的IC任务,随后完成基于实验室的吸烟复发模拟任务。研究1于2008年至2012年在杜克大学医学中心进行;研究2是2013年至2016年在南卡罗莱纳医科大学进行的。皮质丘脑介导的IC、灰质体积和吸烟失效/复发之间的关系。在研究1(戒烟研究)的81名研究参与者中,45名是女性(56%),平均(SD)年龄为38.4(10.2)岁。在研究1中,吸烟复发与灰质体积减少(F1,74 = 28.32;家族误差P阈值= 0.03)、右侧IFG (F1,78 = 14.87)和丘脑(F1,78 = 14.97)的IC任务相关血氧水平依赖性(BOLD)反应增强(P < 0.05)以及皮质丘脑基于任务的功能连接(tbFC)较弱(F1,77 = 5.87; P = 0.02)相关。在研究2(实验室研究)的26名参与者中,15名女性(58%),平均(SD)年龄为34.9岁(10.3岁)。与研究1类似,在研究2中,右侧IFG IC-BOLD反应更强(t23 = - 2.49; β = - 0.47; P = 0.02),皮质丘脑tbFC反应更弱(t22 = 5.62; β = 0.79; P < 0.001)与吸烟复发模拟任务中吸烟更快相关。在这两项研究中,皮质丘脑ttbfc介导了IC表现与吸烟结果之间的关联。在这两项研究中,皮质丘脑回路功能的基线差异与介导的IC和吸烟复发易感性相关。这些发现为进一步研究在烟草使用障碍治疗过程中增强皮质丘脑神经传递和增强IC的干预措施提供了依据。
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. To examine associations between IC neural circuitry structure and function and lapse/relapse vulnerability in 2 independent studies of adult smokers. 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. Associations between corticothalamic-mediated IC, gray-matter volume, and smoking lapse/relapse. 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. 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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