Acetic acid conditioning stimulus induces long-lasting antinociception of somatic inflammatory pain
Acetic acid conditioning stimulus induces long-lasting antinociception of somatic inflammatory pain
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DOI：
10.1016/s0091-3057(03)00014-5
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发表时间：
2003-03-01
影响因子：
3.6
通讯作者：
Tanabe, T
中科院分区：
文献类型：
--
作者：
Kurihara, T;Nonaka, T;Tanabe, T
众所周知，各种各样的有害刺激会对身体偏远区域产生的痛感产生强大的抑制作用。在这里，我们展示了腹膜内醋酸(AA)的条件性刺激对福尔马林诱发的小鼠躯体炎性疼痛行为产生长期的抑制作用。5-羟色胺2A/2C(5-HT2A/2C)受体拮抗剂酮丝氨酸和瑞坦丝林可完全阻断这种新型的长效抗伤害性感觉，但阿片受体拮抗剂纳洛酮和α-肾上腺素能受体拮抗剂酚妥拉明和育亨宾不能阻断这一新的长效抗伤害性感觉。相比之下，5-HT3/4受体拮抗剂托烷司琼显著增强了这种持久的抗伤害性感觉。条件性刺激显著上调延髓色氨酸羟化酶免疫反应性和脊髓5-HT2A/2C受体mRNA水平。这些结果表明，内脏伤害性刺激引起5-羟色胺能抑制系统的持续增强，并下调了躯体炎性伤害性信息传递。(C)2003 Elsevier Science Inc.保留所有权利。
A wide variety of noxious stimuli are known to induce a powerful inhibition of pain sensation evoked at a remote region of the body. Here we show that an intraperitoneal acetic acid (AA) conditioning stimulus produces long-lasting inhibition of formalin-evoked somatic inflammatory pain behavior in mice. This novel long-lasting antinociception was completely blocked by the 5-hydroxytryptamine type 2A/2C (5-HT2A/2C) receptor antagonists, ketanserin and ritanserin, but not by the opioid receptor antagonist, naloxone, and alpha-adrenergic receptor antagonists, phentolamine and yohimbine. In contrast, the 5-HT3/4 receptor antagonist, tropisetron, significantly potentiated this long-lasting antinociception. The conditioning stimulus significantly upregulated the levels of both tryptophan hydroxylase immunoreactivity, in the medulla oblongata and the 5-HT2A/2C receptor mRNA level in the spinal cord. These results suggested that the visceral noxious stimulus caused a long-lasting augmentation of the serotonergic inhibitory system and downregulated the somatic inflammatory nociceptive transmission. (C) 2003 Elsevier Science Inc. All rights reserved.