Department of Psychiatry, University of Michigan, Ann Arbor, MI, USA.
Neuropharmacology. 2013 Jan;64(1):396-402. doi: 10.1016/j.neuropharm.2012.06.063. Epub 2012 Jul 13.
A first-line approach to treat anxiety disorders is exposure-based therapy, which relies on extinction processes such as repeatedly exposing the patient to stimuli (conditioned stimuli; CS) associated with the traumatic, fear-related memory. However, a significant number of patients fail to maintain their gains, partly attributed to the fact that this inhibitory learning and its maintenance is temporary and conditioned fear responses can return. Animal studies have shown that activation of the cannabinoid system during extinction learning enhances fear extinction and its retention. Specifically, CB1 receptor agonists, such as Δ9-tetrahydrocannibinol (THC), can facilitate extinction recall by preventing recovery of extinguished fear in rats. However, this phenomenon has not been investigated in humans. We conducted a study using a randomized, double-blind, placebo-controlled, between-subjects design, coupling a standard Pavlovian fear extinction paradigm and simultaneous skin conductance response (SCR) recording with an acute pharmacological challenge with oral dronabinol (synthetic THC) or placebo (PBO) 2 h prior to extinction learning in 29 healthy adult volunteers (THC = 14; PBO = 15) and tested extinction retention 24 h after extinction learning. Compared to subjects that received PBO, subjects that received THC showed low SCR to a previously extinguished CS when extinction memory recall was tested 24 h after extinction learning, suggesting that THC prevented the recovery of fear. These results provide the first evidence that pharmacological enhancement of extinction learning is feasible in humans using cannabinoid system modulators, which may thus warrant further development and clinical testing. This article is part of a Special Issue entitled 'Cognitive Enhancers'.
治疗焦虑障碍的一线方法是基于暴露的疗法,该疗法依赖于诸如反复使患者暴露于与创伤、恐惧相关的记忆相关的刺激(条件刺激;CS)之类的消除过程。然而,大量患者无法维持其收益,部分原因是这种抑制性学习及其维持是暂时的,条件性恐惧反应可能会恢复。动物研究表明,在消除学习过程中激活大麻素系统可增强恐惧消除及其保留。具体而言,CB1 受体激动剂,如Δ9-四氢大麻酚(THC),可通过防止大鼠中已消除的恐惧恢复,从而促进消除记忆的回忆。但是,尚未在人类中对此现象进行研究。我们进行了一项研究,使用随机,双盲,安慰剂对照,组间设计,将标准的条件恐惧消退范式与同时的皮肤电反应(SCR)记录与急性药理学挑战相结合,在 29 名健康成年志愿者(THC = 14;PBO = 15)中,在消退学习前 2 小时口服给予大麻二酚(合成 THC)或安慰剂(PBO),并在消退学习后 24 小时测试消退保留。与接受 PBO 的受试者相比,接受 THC 的受试者在消退记忆回忆测试时对先前消退的 CS 表现出低 SCR,这表明 THC 阻止了恐惧的恢复。这些结果首次提供了证据,表明使用大麻素系统调节剂可增强人类的消退学习,这可能需要进一步的开发和临床测试。本文是题为“认知增强剂”的特刊的一部分。