Colizzi Marco, McGuire Philip, Giampietro Vincent, Williams Steve, Brammer Mick, Bhattacharyya Sagnik
Department of Psychosis Studies, Institute of Psychiatry, Psychology & Neuroscience, King's College London.
Department of Neuroimaging, Institute of Psychiatry, Psychology & Neuroscience, King's College London.
Exp Clin Psychopharmacol. 2018 Dec;26(6):582-598. doi: 10.1037/pha0000221. Epub 2018 Aug 23.
Cannabis can induce transient psychotic and anxiety symptoms and long-lasting disorders. The acute psychoactive effects of its main active ingredient, (-)-trans-Δ9-tetrahydrocannabinol (Δ9-THC), may be modulated by previous cannabis exposure. Secondary data analyses tested whether modest previous cannabis exposure modulated the acute effects of Δ9-THC on attentional salience and emotional processing and their neurophysiological substrates. Twenty-four healthy men participated in a double-blind, randomized, placebo-controlled, repeated-measures, within-subject, Δ9-THC challenge study using fMRI. Compared with nonusers (NUs; n = 12; <5 lifetime cannabis joints smoked), abstinent-modest cannabis users (CUs; n = 12; 24.5 ± 9 lifetime cannabis joints smoked) showed less efficient attentional salience processing and recruited different/additional brain areas to process attentional salient and emotional stimuli (all ps ≤ .01). The Δ9-THC challenge disrupted attentional salience and emotional-processing-related brain activity and induced transient anxiety and psychotic symptoms (all ps ≤ .02). However, Δ9-THC-induced psychotic symptoms and attentional salience behavioral impairment were more pronounced in NUs compared with CUs (all ps ≤ .04). Also, NUs under Δ9-THC shifted toward recruitment of other brain areas to perform the tasks. Conversely, CUs were less affected by the acute challenge in an exposure-dependent manner, showing a neurophysiological pattern similar to that of NUs under placebo. Only in NUs, Δ9-THC-induced psychotic symptom and cognitive impairment severity was associated with a more pronounced neurophysiological alteration (all ps ≤ .048). In conclusion, CUs displayed residual effects of cannabis exposure but more blunted responses to the acute symptomatic, behavioral, and neurophysiological effects of Δ9-THC, which were more marked in NUs. (PsycINFO Database Record (c) 2018 APA, all rights reserved).
大麻可诱发短暂的精神病性和焦虑症状以及持久性障碍。其主要活性成分（-）-反式-Δ9-四氢大麻酚（Δ9-THC）的急性精神活性作用可能会受到既往大麻接触史的调节。二次数据分析检验了既往适度的大麻接触是否会调节Δ9-THC对注意力突显和情绪加工及其神经生理底物的急性作用。24名健康男性参与了一项使用功能磁共振成像（fMRI）的双盲、随机、安慰剂对照、重复测量、受试者内Δ9-THC激发研究。与非使用者（NUs；n = 12；终生吸食大麻卷烟<5支）相比，戒断的适度大麻使用者（CUs；n = 12；终生吸食大麻卷烟24.5±9支）表现出注意力突显加工效率较低，并且在处理注意力突显和情绪刺激时募集了不同的/额外的脑区（所有p值≤0.01）。Δ9-THC激发破坏了与注意力突显和情绪加工相关的脑活动，并诱发了短暂的焦虑和精神病性症状（所有p值≤0.02）。然而，与CUs相比，Δ9-THC诱发的精神病性症状和注意力突显行为损害在NUs中更为明显（所有p值≤0.04）。此外，接受Δ9-THC的NUs转向募集其他脑区来执行任务。相反，CUs以暴露依赖的方式受急性激发的影响较小，表现出与接受安慰剂的NUs相似的神经生理模式。仅在NUs中，Δ9-THC诱发的精神病性症状和认知损害严重程度与更明显的神经生理改变相关（所有p值≤0.048）。总之，CUs表现出大麻接触的残留效应，但对Δ9-THC的急性症状、行为和神经生理作用的反应更为迟钝，而这些在NUs中更为明显。（《心理学文摘数据库记录》（c）2018美国心理学会，保留所有权利）
