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首页> 外文期刊>Physiological Reviews >Sensory and signaling mechanisms of bradykinin, eicosanoids, platelet-activating factor, and nitric oxide in peripheral nociceptors
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Sensory and signaling mechanisms of bradykinin, eicosanoids, platelet-activating factor, and nitric oxide in peripheral nociceptors

机译：周围伤害感受器中缓激肽，类花生酸，血小板活化因子和一氧化氮的感觉和信号传导机制

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Peripheral mediators can contribute to the development and maintenance of inflammatory and neuropathic pain and its concomitants (hyperalgesia and allodynia) via two mechanisms. Activation or excitation by these substances of nociceptive nerve endings or fibers implicates generation of action potentials which then travel to the central nervous system and may induce pain sensation. Sensitization of nociceptors refers to their increased responsiveness to either thermal, mechanical, or chemical stimuli that may be translated to corresponding hyperalgesias. This review aims to give an account of the excitatory and sensitizing actions of inflammatory mediators including bradykinin, prostaglandins, thromboxanes, leukotrienes, platelet-activating factor, and nitric oxide on nociceptive primary afferent neurons. Manifestations, receptor molecules, and intracellular signaling mechanisms of the effects of these mediators are discussed in detail. With regard to signaling, most data reported have been obtained from transfected nonneuronal cells and somata of cultured sensory neurons as these structures are more accessible to direct study of sensory and signal transduction. The peripheral processes of sensory neurons, where painful stimuli actually affect the nociceptors in vivo, show marked differences with respect to biophysics, ultrastructure, and equipment with receptors and ion channels compared with cellular models. Therefore, an effort was made to highlight signaling mechanisms for which supporting data from molecular, cellular, and behavioral models are consistent with findings that reflect properties of peripheral nociceptive nerve endings. Identified molecular elements of these signaling pathways may serve as validated targets for development of novel types of analgesic drugs.
机译：周围介质可通过两种机制促进炎性和神经性疼痛及其伴随疾病（痛觉过敏和异常性疼痛）的发展和维持。这些物质对伤害性神经末梢或纤维的激活或激发牵涉到动作电位的产生，然后该动作电位传播至中枢神经系统并可能引起疼痛感。伤害感受器的敏化作用是指它们对可能转换为相应痛觉过敏的热，机械或化学刺激的反应性增强。这篇综述旨在说明包括缓激肽，前列腺素，血栓烷，白三烯，血小板活化因子和一氧化氮在内的炎性介质对伤害性原发传入神经元的兴奋性和敏化作用。详细讨论了这些介体作用的表现，受体分子和细胞内信号传导机制。关于信号，报告的大多数数据是从培养的感觉神经元的转染非神经元细胞和躯体获得的，因为这些结构更容易直接用于感觉和信号转导研究。与细胞模型相比，感觉神经元的周围过程（其中疼痛的刺激实际上影响体内的伤害感受器）在生物物理学，超微结构以及带有受体和离子通道的设备方面表现出明显差异。因此，努力强调信号传导机制，其分子，细胞和行为模型的支持数据与反映外周伤害性神经末梢特性的发现一致。这些信号通路的分子元素可以作为开发新型镇痛药的有效靶点。

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