New insights into the mechanisms of itch: are pain and itch controlled by distinct mechanisms?
New insights into the mechanisms of itch: are pain and itch controlled by distinct mechanisms?
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DOI：
10.1007/s00424-013-1284-2
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发表时间：
2013-12
影响因子：
4.5
通讯作者：
Ji, Ru-Rong
中科院分区：
文献类型：
--
作者：
Liu, Tong;Ji, Ru-Rong
关键词：
痒和痛是密切相关但又截然不同的感觉。它们有很多重叠的介质和受体，瘙痒反应神经元对疼痛刺激也很敏感。瘙痒介导的初级感觉神经元具有不同的瘙痒转导受体和离子通道，包括mas相关G蛋白偶联受体（Mrgprs）、蛋白酶激活受体（PARs）、组胺受体、胆酸受体（TGR5）、toll样受体（TLRs）和瞬时受体电位亚家族V1/A1 （TRPV1/A1）。最近的进展表明，存在一种针对瘙痒的神经回路。表达mrgpra3的初级感觉神经元独占支配皮肤表皮，其中央轴突与脊髓浅表表达胃泌素释放肽受体（GRPR）的神经元连接。值得注意的是，消融表达mrgpra3的初级感觉神经元或表达grpr的脊髓神经元导致瘙痒选择性减少，而不是疼痛。慢性瘙痒是免疫和神经系统功能障碍的结果，可以表现为神经可塑性，尽管慢性瘙痒通常由皮肤科医生治疗。虽然急性疼痛和急性瘙痒之间的差异是显著的，但慢性瘙痒和慢性疼痛有许多相似的机制，包括外周致敏（初级感觉神经元对瘙痒和疼痛介质的反应增加），中枢致敏（脊髓投射神经元和兴奋性中间神经元的过度活跃），脊髓抑制控制的丧失，以及神经免疫和神经胶质的相互作用。值得注意的是，在一些慢性疾病（如特应性皮炎）中，疼痛刺激可引起瘙痒，一些治疗慢性疼痛的药物对慢性瘙痒也有效。因此，瘙痒和疼痛在病理和慢性条件下有更多的相似之处。
Itch and pain are closely related but distinct sensations. They share largely overlapping mediators and receptors, and itch-responding neurons are also sensitive to pain stimuli. Itch-mediating primary sensory neurons are equipped with distinct receptors and ion channels for itch transduction, including Mas-related G protein-coupled receptors (Mrgprs), protease-activated receptors (PARs), histamine receptors, bile acid receptor (TGR5), toll-like receptors (TLRs), and transient receptor potential subfamily V1/A1 (TRPV1/A1). Recent progress has indicated the existence of an itch-specific neuronal circuitry. The MrgprA3-expressing primary sensory neurons exclusively innervate the epidermis of skin and their central axons connect with gastrin-releasing peptide receptor (GRPR)-expressing neurons in the superficial spinal cord. Notably, ablation of MrgprA3-expressing primary sensory neurons or GRPR-expressing spinal cord neurons results in selective reduction in itch but not pain. Chronic itch results from dysfunction of the immune and nervous system and can manifest as neural plasticity, despite the fact that chronic itch is often treated by dermatologists. While differences between acute pain and acute itch are striking, chronic itch and chronic pain share many similar mechanisms, including peripheral sensitization (increased responses of primary sensory neurons to itch and pain mediators), central sensitization (hyperactivity of spinal projection neurons and excitatory interneurons), loss of inhibitory control in the spinal cord, and neuro-immune and neuro-glial interactions. Notably, painful stimuli can elicit itch in some chronic conditions (e.g., atopic dermatitis) and some drugs for treating chronic pain are also effective in chronic itch. Thus, itch and pain have more similarities in pathological and chronic conditions.
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