Bamford Susan, Penton-Voak Ian, Pinkney Verity, Baldwin David S, Munafò Marcus R, Garner Matthew
School of Psychology, University of Southampton, Southampton, UK.
School of Experimental Psychology, University of Bristol, Bristol, UK.
J Psychopharmacol. 2015 May;29(5):634-41. doi: 10.1177/0269881115570085. Epub 2015 Mar 10.
The serotonin-noradrenaline reuptake inhibitor (SNRI) duloxetine is an effective treatment for major depression and generalised anxiety disorder. Neuropsychological models of antidepressant drug action suggest therapeutic effects might be mediated by the early correction of maladaptive biases in emotion processing, including the recognition of emotional expressions. Sub-chronic administration of duloxetine (for two weeks) produces adaptive changes in neural circuitry implicated in emotion processing; however, its effects on emotional expression recognition are unknown. Forty healthy participants were randomised to receive either 14 days of duloxetine (60 mg/day, titrated from 30 mg after three days) or matched placebo (with sham titration) in a double-blind, between-groups, repeated-measures design. On day 0 and day 14 participants completed a computerised emotional expression recognition task that measured sensitivity to the six primary emotions. Thirty-eight participants (19 per group) completed their course of tablets and were included in the analysis. Results provide evidence that duloxetine, compared to placebo, may reduce the accurate recognition of sadness. Drug effects were driven by changes in participants' ability to correctly detect subtle expressions of sadness, with greater change observed in the placebo relative to the duloxetine group. These effects occurred in the absence of changes in mood. Our preliminary findings require replication, but complement recent evidence that sadness recognition is a therapeutic target in major depression, and a mechanism through which SNRIs could resolve negative biases in emotion processing to achieve therapeutic effects.
5-羟色胺-去甲肾上腺素再摄取抑制剂(SNRI)度洛西汀是治疗重度抑郁症和广泛性焦虑症的有效药物。抗抑郁药物作用的神经心理学模型表明,治疗效果可能是通过早期纠正情绪加工中的适应不良偏差来介导的,包括对情绪表达的识别。亚慢性给予度洛西汀(持续两周)会使与情绪加工相关的神经回路产生适应性变化;然而,其对情绪表达识别的影响尚不清楚。40名健康参与者被随机分为两组,在双盲、组间、重复测量设计中,一组接受14天的度洛西汀治疗(60毫克/天,三天后从30毫克开始滴定),另一组接受匹配的安慰剂治疗(假滴定)。在第0天和第14天,参与者完成了一项计算机化的情绪表达识别任务,该任务测量了对六种基本情绪的敏感性。38名参与者(每组19名)完成了片剂疗程并被纳入分析。结果表明,与安慰剂相比,度洛西汀可能会降低对悲伤情绪的准确识别。药物效应是由参与者正确检测悲伤细微表情的能力变化驱动的,安慰剂组相对于度洛西汀组观察到更大的变化。这些效应在情绪没有变化的情况下出现。我们的初步研究结果需要重复验证,但补充了最近的证据,即悲伤识别是重度抑郁症的一个治疗靶点,也是SNRIs可以解决情绪加工中的负面偏差以实现治疗效果的一种机制。