Stress-induced enhancement of response inhibition depends on mineralocorticoid receptor activation
Stress-induced enhancement of response inhibition depends on mineralocorticoid receptor activation
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DOI：
10.1016/j.psyneuen.2013.05.001
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发表时间：
2013-10-01
影响因子：
3.7
通讯作者：
Wolf, Oliver T.
中科院分区：
文献类型：
--
作者：
Schwabe, Lars;Hoeffken, Oliver;Wolf, Oliver T.
压力是认知功能的一种众所周知的调节剂。这些作用至少部分是由糖皮质激素应激激素介导的，糖皮质激素应激激素通过大脑中的两种受体类型（糖皮质激素受体（GR）和盐皮质激素受体（MR））发挥作用。在这里，我们研究了压力是否会影响抑制控制过程，如果是这样，这些影响是否是由MR介导的。为此，健康参与者接受了300毫克的MR拮抗剂螺内酯或安慰剂，并进行了应激源（社会评价冷加压试验）或非压力控制任务90分钟后。在压力源之后不久，参与者执行了一项停止信号任务，要求他们在出现音调时迅速抑制一个既定的反应。结果表明，压力增强反应抑制停止信号的任务，这种增强被螺内酯取消。我们的研究结果表明，压力可能有助于抑制控制，这些影响取决于MR功能。(C)2013爱思唯尔有限公司保留所有权利。
Stress is a well-known modulator of cognitive functions. These effects are, at least in part, mediated by glucocorticoid stress hormones which act via two receptor types in the brain, glucocorticoid receptors (GR) and mineralocorticoid receptors (MR). Here, we examined whether stress affects inhibitory control processes and, if so, whether these effects are mediated by the MR. To this end, healthy participants received 300 mg of the MR antagonist spironolactone or a placebo and underwent a stressor (socially evaluated cold pressor test) or a non-stressful control task 90 min later. Shortly after the stressor, participants performed a stop-signal task that required them to rapidly suppress a well-established response whenever a tone was presented. Results revealed that stress enhanced response inhibition in the stop-signal task and that this enhancement was abolished by spironolactone. Our results show that stress may facilitate inhibitory control and that these effects depend on MR functioning. (C) 2013 Elsevier Ltd. All rights reserved.