摘要
ATP是广泛存在于周围和中枢神经系统的神经递质。自损伤细胞或炎症组织释放至细胞外的ATP可激活初级传入神经元上的P2X和P2Y受体,引起疼痛。P2X受体中的P2X3亚单位高度选择性表达于感觉神经元,应用P2X3受体反义寡核苷酸、RNA干扰、基因敲除技术和选择性拮抗剂等研究表明,ATP和P2X3受体在多种疼痛的产生和维持中起重要作用。PGE2、NGF、SP和谷氨酸等可增强P2X3受体激动剂激发的内向电流,对P2X3受体的功能起急性上调作用。但是在一些慢性疼痛模型中,P2X3受体表达上调和活性增加的机制并不十分清楚。
ATP is a neurotransmitter which generally resides in peripheral and central nervous system. ATP released from damaged or inflamed tissues can act at P2X and P2Y receptors, which can evoke pain. P2X3 subunit from P2X receptor is found in a subset of small- and medium-size primary afferent neurons. Experiments with antisense oligonucleotides to reduce P2X3 subunit levels, or with short interfering RNAs to decrease with antagonists selective forming and signaling of P2X3 subunit levels, behavioural testing in P2X3 knock-out mice, and studies for P2X3 receptor, all suggest an important role for the P2X3 receptor in the acute and chronic inflammatory pain and some features of neuropathie pain. PGE2, NGF, SP and Glut can increase P2X3 receptor-mediated currents and enhance the function of P2X3 receptor. However, the mechanisms of expressive and functional upregulation of P2X3 receptor subunit in chronic pain models still remain unclear.
出处
《中国疼痛医学杂志》
CAS
CSCD
2009年第3期177-180,共4页
Chinese Journal of Pain Medicine
基金
中南大学大学生创新性实验计划项目(YA07067)
