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应激诱导的痛觉过敏。

Stress-induced hyperalgesia.

作者信息

Jennings Elaine M, Okine Bright N, Roche Michelle, Finn David P

机构信息

Pharmacology and Therapeutics, School of Medicine, National University of Ireland, Galway, Ireland; NCBES Centre for Pain Research and Galway Neuroscience Centre, National University of Ireland, Galway, Ireland.

NCBES Centre for Pain Research and Galway Neuroscience Centre, National University of Ireland, Galway, Ireland; Physiology, School of Medicine, National University of Ireland, Galway, Ireland.

出版信息

Prog Neurobiol. 2014 Oct;121:1-18. doi: 10.1016/j.pneurobio.2014.06.003. Epub 2014 Jul 8.

DOI:10.1016/j.pneurobio.2014.06.003
PMID:25010858
Abstract

The importance of the modulation of pain by emotion is now widely recognised. In particular, stress and anxiety, depending on their nature, duration and intensity, can exert potent, but complex, modulatory influences typified by either a reduction or exacerbation of the pain state. Exposure to either acute or chronic stress can increase pain responding under experimental conditions and exacerbate clinical pain disorders. There is evidence that exposure to chronic or repeated stress can produce maladaptive neurobiological changes in pathways associated with pain processing, resulting in stress-induced hyperalgesia (SIH). Preclinical studies of SIH are essential for our understanding of the mechanisms underpinning stress-related pain syndromes and for the identification of neural pathways and substrates, and the development of novel therapeutic agents for their clinical management. In this review, we describe clinical and pre-clinical models used to study SIH and discuss the neural substrates, neurotransmitters and neuromodulatory systems involved in this phenomenon.

摘要

情绪对疼痛的调节作用如今已得到广泛认可。特别是压力和焦虑,根据其性质、持续时间和强度,会产生强大但复杂的调节影响,表现为疼痛状态的减轻或加剧。在实验条件下,暴露于急性或慢性压力均可增加疼痛反应,并加重临床疼痛障碍。有证据表明,暴露于慢性或反复的压力会在与疼痛处理相关的通路中产生适应不良的神经生物学变化,导致应激诱导的痛觉过敏(SIH)。SIH的临床前研究对于我们理解与压力相关的疼痛综合征的潜在机制、识别神经通路和底物以及开发用于其临床管理的新型治疗药物至关重要。在本综述中,我们描述了用于研究SIH的临床和临床前模型,并讨论了参与这一现象的神经底物、神经递质和神经调节系统。

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