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急性不可逃避应激可缓解由5-羟色胺转运体缺失所导致的恐惧消退记忆缺陷。

Acute inescapable stress alleviates fear extinction recall deficits caused by serotonin transporter abolishment.

作者信息

Schipper Pieter, Henckens Marloes J A G, Lopresto Dora, Kozicz Tamas, Homberg Judith R

机构信息

Department of Cognitive Neuroscience, Centre for Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboudumc, Geert Grooteplein 21 (Route 126), 6525 EZ Nijmegen, The Netherlands.

Anatomy Department, Centre for Neuroscience, Donders Institute for Brain, Cognition and Behaviour, Radboudumc, Geert Grooteplein 21 (Route 109), 6525 EZ Nijmegen, The Netherlands.

出版信息

Behav Brain Res. 2018 Jul 2;346:16-20. doi: 10.1016/j.bbr.2017.12.009. Epub 2017 Dec 9.

Abstract

Life stress increases risk for developing post-traumatic stress disorder (PTSD), and more prominently so in short-allele carriers of the serotonin transporter linked polymorphic region (5-HTTLPR). Serotonin transporter knockout (5-HTT) rats show compromised extinction (recall) of conditioned fear, which might mediate the increased risk for PTSD and reduce the therapeutic efficacy of exposure therapy. Here, we assessed whether acute inescapable stress (IS) differentially affects fear extinction and extinction recall in 5-HTT rats and wildtype controls. Surprisingly, IS experience improved fear extinction recall in 5-HTT rats to the level of wildtype animals, while wildtypes were unaffected by this IS. Thus, whereas 5-HTT rats evidently were more responsive to the stressor, the behavioral consequences presented themselves as adaptive.

摘要

生活压力会增加患创伤后应激障碍(PTSD)的风险,对于携带血清素转运体相关多态性区域(5-HTTLPR)短等位基因的个体而言,这种风险增加更为显著。血清素转运体基因敲除(5-HTT)大鼠在条件性恐惧的消退(回忆)方面存在缺陷,这可能介导了PTSD风险的增加,并降低暴露疗法的治疗效果。在此,我们评估了急性不可逃避应激(IS)是否会对5-HTT大鼠和野生型对照的恐惧消退及消退回忆产生不同影响。令人惊讶的是,经历IS后,5-HTT大鼠的恐惧消退回忆改善至野生型动物的水平,而野生型大鼠则不受此IS影响。因此,尽管5-HTT大鼠显然对压力源反应更强,但行为结果却表现为适应性的。

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