摘要
疼痛是一个复杂的多维概念，有助于响应任何有害刺激启动信号级联反应。外周伤害感受器终端中的动作电位产生及其通过对应于机械，化学或热刺激的各种类型的伤害感受器的传递导致受体的激活，并且进一步的神经元处理产生疼痛的感觉。许多类型的受体在疼痛感觉中被激活，其信号传导途径不同。这些信号传导途径可以被认为是通过靶向疼痛转导分子产生镇痛来调节疼痛的部位。基于它们的解剖位置，瞬时受体电位离子通道（TRPV1，TRPV2和TRPM8），Piezo 2，酸敏感离子通道（ASIC），嘌呤能（P2X和P2Y），缓激肽（B1和B2），α-氨基-3-羟基-5-甲基异恶唑-4-丙酸酯（AMPA），N-甲基-D-天冬氨酸（NMDA），代谢型谷氨酸（mGlu），神经激肽1（NK1）和降钙素基因相关肽（CGRP）受体被激活在疼痛过敏期间。 TRPV1，TRPV2，TRPM8，Piezo2，ASICs，P2X，P2Y，B1，B2，AMPA，NMDA，mGlu，NK1和CGRP受体的各种抑制剂在疼痛的实验模型中显示出高治疗价值。类似地，通过激活阿片类，肾上腺素能，5-羟色胺能和大麻素受体的局部抑制调节已经通过调节疼痛刺激的中枢和外周感知显示出镇痛特性。该综述主要关注疼痛转导，传递和调节中涉及的各类伤害感受器，疼痛传递途径中的伤害感受器的作用部位以及通过利用伤害感受器减轻疼痛刺激的药物（临床和临床前数据，与靶标相关）。特定的通道和受体。
关键词: 疼痛调节受体，疼痛传递途径，疼痛药理学靶标，脑和脊髓，伤害感受器致敏，N-甲基-D-天冬氨酸（NMDA）。
图形摘要
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