Immobilization stress-induced anorexia is mediated independent of MyD88

被引：0
作者：
Hosoi, Toru [1 ]
Yamawaki, Yosuke [2 ]
Kimura, Hitomi [1 ]
Ozawa, Koichiro [1 ]
机构：
[1] Hiroshima Univ, Grad Sch Biomed & Hlth Sci, Dept Pharmacotherapy, Hiroshima 7348553, Japan
[2] Hiroshima Univ, Dept Cellular & Mol Pharmacol, Inst Biomed & Hlth Sci, Hiroshima 7348553, Japan
来源：
NEUROREPORT | 2016年 / 27卷 / 13期
关键词：
anorexia; immobilization stress; MyD88; STAT3; ACTIVATION; FOOD-INTAKE; BRAIN; INTERLEUKIN-1-BETA; HYPOTHALAMUS; CYTOKINES; ENDOTOXIN; EXPOSURE; RECEPTOR; LEPTIN;
D O I：
10.1097/WNR.0000000000000641
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
MyD88 is an adaptor protein for the toll-like receptor, which is involved in regulating innate immune function. Lipopolysaccharide-induced activation of toll-like receptor 4 signaling induces hypothalamic signal transducer and activator of transcription 3 (STAT3) phosphorylation and anorexia through MyD88. In the present study, we investigated the possible role of MyD88 in psychological stress-induced anorexia. We found that immobilization stress inhibited food intake in both wild-type mice and MyD88-deficient mice. Immobilization stress slightly increased STAT3 phosphorylation in the hypothalamus, but it was weaker than the lipopolysaccharide-induced increase in STAT3 phosphorylation. These observations suggest that the mechanisms involved in psychological stress-induced anorexia may be regulated differently from those involved in anorexia that is induced by infection. Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.
引用
收藏
页码：974 / 977
页数：4
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