Activation of ERK in the rostral ventromedial medulla is involved in hyperalgesia during peripheral inflammation

被引：15

作者：

Imbe, Hiroki ^{[1
]}

Kimura, Akihisa ^{[1
]}

Okamoto, Keiichiro ^{[2
]}

Donishi, Tomohiro ^{[1
]}

Aikawa, Fumiko ^{[3
]}

Senba, Emiko ^{[4
]}

Tamai, Yasuhiko ^{[1
]}

机构：

[1] Wakayama Med Univ, Dept Physiol, Wakayama 6418509, Japan

[2] Univ Minnesota, Sch Dent, Dept Diagnost & Biol Sci, Minneapolis, MN 55455 USA

[3] Osaka Dent Univ, Dept Oral Anat, Hirakata, Osaka 5731121, Japan

[4] Wakayama Med Univ, Dept Anat & Neurobiol, Wakayama, Japan

来源：

BRAIN RESEARCH | 2008年 / 1187卷

关键词：

descending system; inflammation; ERK; hyperalgesia;

D O I：

10.1016/j.brainres.2007.10.075

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

We have previously shown that the extracellular signal-regulated kinase (ERK) is activated in the rostral ventromedial medulla (RVM) during peripheral inflammation. In the present study, the relationship between ERK signaling in the RVM and pain hypersensitivity was investigated in the rat. Microinjection of U0126, a mitogen-activated protein kinase kinase inhibitor, into the RVM decreased phosphorylated ERK at 7 h after complete Freund's adjuvant (CFA) injection into the hindpaw. The U0126 microinjection also attenuated thermal hyperalgesia in the ipsilateral hindpaw at 24 h after CFA injection. The ipsilateral paw withdrawal latency in the U0126 group (67.9%+/- 5.3% vs. baseline, n = 7) was significantly longer than that in the control group (52.0%+/- 3.6% vs. baseline, n = 8). These findings suggest that activation of ERK in the RVM contributes to thermal hyperalgesia. during peripheral inflammation. (c) 2007 Elsevier B.V. All rights reserved.

引用

页码：103 / 110

页数：8

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