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痛觉过敏和异常性疼痛的模型与机制。

Models and mechanisms of hyperalgesia and allodynia.

作者信息

Sandkühler Jürgen

机构信息

Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.

出版信息

Physiol Rev. 2009 Apr;89(2):707-58. doi: 10.1152/physrev.00025.2008.

Abstract

Hyperalgesia and allodynia are frequent symptoms of disease and may be useful adaptations to protect vulnerable tissues. Both may, however, also emerge as diseases in their own right. Considerable progress has been made in developing clinically relevant animal models for identifying the most significant underlying mechanisms. This review deals with experimental models that are currently used to measure (sect. II) or to induce (sect. III) hyperalgesia and allodynia in animals. Induction and expression of hyperalgesia and allodynia are context sensitive. This is discussed in section IV. Neuronal and nonneuronal cell populations have been identified that are indispensable for the induction and/or the expression of hyperalgesia and allodynia as summarized in section V. This review focuses on highly topical spinal mechanisms of hyperalgesia and allodynia including intrinsic and synaptic plasticity, the modulation of inhibitory control (sect. VI), and neuroimmune interactions (sect. VII). The scientific use of language improves also in the field of pain research. Refined definitions of some technical terms including the new definitions of hyperalgesia and allodynia by the International Association for the Study of Pain are illustrated and annotated in section I.

摘要

痛觉过敏和痛觉异常是常见的病症症状,可能是保护脆弱组织的有益适应性反应。然而,它们自身也可能发展成为疾病。在开发用于确定最重要潜在机制的临床相关动物模型方面已经取得了相当大的进展。本综述涉及目前用于测量(第二节)或诱导(第三节)动物痛觉过敏和痛觉异常的实验模型。痛觉过敏和痛觉异常的诱导和表现具有情境敏感性。这将在第四节中讨论。第五节总结了已确定的对于痛觉过敏和痛觉异常的诱导和/或表现不可或缺的神经元和非神经元细胞群。本综述重点关注痛觉过敏和痛觉异常高度相关的脊髓机制,包括内在和突触可塑性、抑制性控制的调节(第六节)以及神经免疫相互作用(第七节)。在疼痛研究领域,语言的科学运用也有所改进。第一节阐述并注释了一些技术术语的精确定义,包括国际疼痛研究协会对痛觉过敏和痛觉异常的新定义。

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