Role of N-methyl-D-aspartate receptors and the nitric oxide pathway in nociception/hyperalgesia elicited by protease-activated receptor-2 activation in mice and rats
Role of N-methyl-D-aspartate receptors and the nitric oxide pathway in nociception/hyperalgesia elicited by protease-activated receptor-2 activation in mice and rats
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DOI：
10.1016/s0304-3940(02)00702-4
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发表时间：
2002-09-06
影响因子：
2.5
通讯作者：
Ogawa, S
中科院分区：
文献类型：
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作者：
Kawabata, A;Kawao, N;Ogawa, S
外周蛋白酶激活受体2（PAR-2）的激活触发大鼠的伤害性行为和热痛觉过敏。本研究建立了一种新的PAR-2诱发的小鼠伤害性感受模型，并研究了NMIDA受体和一氧化氮（NO）通路在PAR-2诱发的伤害性感受过程中的作用。PAR-2激动剂SLIGRL-NH 2的足底给药引起小鼠的伤害性反应，这种作用在肥大细胞耗竭的小鼠中更具特异性。NMDA受体拮抗剂MK-801可阻断PAR-2引起的伤害性感受，而神经元型NO合酶抑制剂7-硝基吲唑则不能阻断PAR-2引起的伤害性感受。相反，PAR-2触发的大鼠热痛觉过敏被两种药物阻断。因此，我们的研究提供了一种新的小鼠模型PAR-2介导的伤害性感受，并表明，NMDA受体参与PAR-2触发的伤害性感受和痛觉过敏，而NO只有助于后者。(C)2002年由Elsevier Science爱尔兰有限公司出版。
Activation of the peripheral protease-activated receptor-2 (PAR-2) triggers nociceptive behaviour and thermal hyperalgesia in rats. The present study created a novel mouse model for PAR-2-triggered nociception, and then examined the roles of NMIDA receptors and the nitric oxide (NO) pathway in nociceptive processing by PAR-2. Intraplantar administration of the PAR-2 agonist SLIGRL-NH2 elicited nociceptive responses in mice, an effect being more specific in mast cell-depleted mice. This PAR-2-triggered nociception was abolished by the NMDA receptor antagonist MK-801, but not the neuronal NO synthase inhibitor 7-nitro indazole. In contrast, the PAR-2-triggered thermal hyperalgesia in rats was blocked by both agents. Our study thus provides a novel mouse model for PAR-2-mediated nociception, and suggests that NMDA receptors are involved in PAR-2-triggered nociception and hyperalgesia, while NO contributes only to the latter. (C) 2002 Published by Elsevier Science Ireland Ltd.