Heat Pain and Cold Pain

F. Viana, T. Voets
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引用次数: 13

Abstract

Noxious cold and noxious heat have detrimental effects on key biological macromolecules and thus on the integrity of cells, tissues, and organisms. Thanks to the action of a subset of somatosensory neurons, mammals can swiftly detect noxiously cold or hot objects or environments. These temperature-sensitive nociceptor neurons become activated when the temperature at their free endings in the skin or mucosae reaches noxious levels, provoking acute pain and rapid avoidance reflexes. Whereas acute temperature-induced pain is essential to prevent or limit burn injury, pathological conditions such as inflammation or tissue injury can deregulate the thermal sensitivity of the somatosensory system, resulting in painful dysesthesias such as heat and cold hypersensitivity. In recent years, important advances have been made in our understanding of the cellular and molecular mechanisms that underlie the detection of painful heat or cold. These research efforts not only provided key insights into an evolutionary conserved biological alarm system, but also revealed new avenues for the development of novel therapies to treat various forms of persistent pain.
热痛和冷痛
毒冷和毒热对关键的生物大分子产生有害影响,从而影响细胞、组织和生物体的完整性。由于体感神经元子集的作用,哺乳动物可以迅速检测到有害的冷或热的物体或环境。当皮肤或粘膜自由末端的温度达到有害水平时,这些对温度敏感的伤害感受器神经元就会被激活,引发急性疼痛和快速回避反射。虽然急性温度引起的疼痛对于预防或限制烧伤是必不可少的,但炎症或组织损伤等病理条件可以解除体感觉系统的热敏性,导致疼痛的感觉障碍,如热和冷超敏反应。近年来,我们对细胞和分子机制的理解取得了重要进展,这些机制是检测疼痛的热或冷的基础。这些研究成果不仅为进化保守的生物报警系统提供了关键的见解,而且为开发治疗各种形式的持续性疼痛的新疗法提供了新的途径。
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