Dakhili Amirhossein, Sangchooli Arshiya, Jafakesh Sara, Zare-Bidoky Mehran, Soleimani Ghazaleh, Batouli Seyed Amir Hossein, Kazemi Kamran, Faghiri Ashkan, Oghabian Mohammad Ali, Ekhtiari Hamed
Neuroimaging and Analysis Group. (NIAG), Research Center for Molecular and Cellular Imaging, Tehran University of Medical Sciences, Tehran Iran; Medical Physics Department, Iran University of Medical Sciences, Tehran, Iran.
Iranian National Center for Addiction Studies (INCAS), Tehran University of Medical Science, Tehran, Iran.
Drug Alcohol Depend. 2022 Apr 1;233:109353. doi: 10.1016/j.drugalcdep.2022.109353. Epub 2022 Feb 11.
Drug-related cue-reactivity, dysfunctional negative emotion processing, and response-disinhibition constitute three core aspects of methamphetamine use disorder (MUD). These phenomena have been studied independently, but the neuroscientific literature on their interaction in addictive disorders remains scant.
62 individuals with MUD were scanned when responding to the geometric Go or No-Go cues superimposed over blank, neutral, negative-emotional and drug-related background images. Neural correlates of drug and negative-emotional cue-reactivity, response-inhibition and their interactions were estimated, and methamphetamine cue-reactivity was compared between individuals with MUD and 23 healthy controls. Relationships between behavioral characteristics and observed activations were investigated.
Individuals with MUD had longer reaction times and more errors in drug and negative-emotional compared to blank blocks, and more omission errors in drug compared to neutral blocks. They showed higher drug cue-reactivity than controls across prefrontal, fusiform, and visual regions (Z > 3.1, p-corrected<0.05). Response-inhibition was associated with precuneal, inferior parietal, anterior cingulate, temporal, and inferior frontal activations (Z > 3.1, p-corrected<0.05). Response-inhibition in drug cue blocks coincided with higher activations in the visual cortex and lower activations in the paracentral lobule and superior and inferior frontal gyri, while inhibition during negative-emotional blocks led to higher superior parietal, fusiform, and lateral occipital activations (Z > 3.1, p-corrected<0.05).
Drug cue-reactivity may impair response inhibition partly through activating dis-inhibitory regions, while temporal and parietal activations associated with response-inhibition in negative blocks suggest compensatory activity. Results suggest that drug and negative-emotional cue-reactivity influence response-inhibition, and the study of these interactions may aid mechanistic understanding of methamphetamine use disorder.
与药物相关的线索反应性、功能失调的负性情绪加工和反应抑制构成了甲基苯丙胺使用障碍(MUD)的三个核心方面。这些现象已被分别研究,但关于它们在成瘾性障碍中相互作用的神经科学文献仍然很少。
62名患有MUD的个体在对叠加在空白、中性、负性情绪和与药物相关的背景图像上的几何“执行”或“不执行”线索做出反应时接受扫描。估计药物和负性情绪线索反应性、反应抑制及其相互作用的神经相关性,并比较患有MUD的个体与23名健康对照者之间的甲基苯丙胺线索反应性。研究行为特征与观察到的激活之间的关系。
与空白组相比,患有MUD的个体在药物和负性情绪组中的反应时间更长,错误更多,与中性组相比,在药物组中的漏报错误更多。他们在前额叶、梭状回和视觉区域表现出比对照组更高的药物线索反应性(Z>3.1,校正后p<0.05)。反应抑制与楔前叶、顶下叶、前扣带回、颞叶和额下回的激活有关(Z>3.1,校正后p<0.05)。药物线索组中的反应抑制与视觉皮层中更高的激活以及中央旁小叶和额上回及额下回中更低的激活同时出现,而负性情绪组中的抑制导致顶叶上部、梭状回和枕外侧更高的激活(Z>3.1,校正后p<0.05)。
药物线索反应性可能部分通过激活去抑制区域来损害反应抑制,而与负性组中反应抑制相关的颞叶和顶叶激活提示了代偿性活动。结果表明,药物和负性情绪线索反应性影响反应抑制,对这些相互作用的研究可能有助于对甲基苯丙胺使用障碍的机制理解。