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本文引用的文献

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Tumor necrosis factor-alpha induces neurotoxicity via glutamate release from hemichannels of activated microglia in an autocrine manner.肿瘤坏死因子-α通过激活的小胶质细胞半通道以自分泌方式释放谷氨酸来诱导神经毒性。
J Biol Chem. 2006 Jul 28;281(30):21362-21368. doi: 10.1074/jbc.M600504200. Epub 2006 May 23.
2
TNFalpha signaling in depression and anxiety: behavioral consequences of individual receptor targeting.肿瘤坏死因子α信号通路在抑郁和焦虑中的作用：靶向单个受体的行为后果
Biol Psychiatry. 2006 May 1;59(9):775-85. doi: 10.1016/j.biopsych.2005.10.013. Epub 2006 Feb 3.
3
Effects of insulin-like growth factor-I on cytokine-induced sickness behavior in mice.胰岛素样生长因子-I对小鼠细胞因子诱导的疾病行为的影响。
Brain Behav Immun. 2006 Jan;20(1):57-63. doi: 10.1016/j.bbi.2005.02.003.
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Metabotropic glutamate receptors mediate lipopolysaccharide-induced fever and sickness behavior.代谢型谷氨酸受体介导脂多糖诱导的发热和疾病行为。
Brain Behav Immun. 2006 May;20(3):233-45. doi: 10.1016/j.bbi.2005.08.007. Epub 2005 Oct 20.
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Inhibition of vagally mediated immune-to-brain signaling by vanadyl sulfate speeds recovery from sickness.硫酸氧钒对迷走神经介导的免疫-脑信号传导的抑制作用可加速疾病康复。
Proc Natl Acad Sci U S A. 2005 Oct 18;102(42):15184-9. doi: 10.1073/pnas.0507191102. Epub 2005 Oct 10.
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Pentoxifylline and insulin-like growth factor-I (IGF-I) abrogate kainic acid-induced cognitive impairment in mice.
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7
Central administration of IGF-I and BDNF leads to long-lasting antidepressant-like effects.向中枢给予胰岛素样生长因子-1（IGF-I）和脑源性神经营养因子（BDNF）会产生持久的抗抑郁样效应。
Brain Res. 2005 Mar 10;1037(1-2):204-8. doi: 10.1016/j.brainres.2005.01.007.
8
Cytokine-induced sickness behaviour: a neuroimmune response to activation of innate immunity.细胞因子诱导的疾病行为：对先天免疫激活的神经免疫反应。
Eur J Pharmacol. 2004 Oct 1;500(1-3):399-411. doi: 10.1016/j.ejphar.2004.07.040.
9
Two tumour necrosis factor receptors: structure and function.两种肿瘤坏死因子受体：结构与功能
Trends Cell Biol. 1995 Oct;5(10):392-9. doi: 10.1016/s0962-8924(00)89088-1.
10
Innate immunity at the forefront of psychoneuroimmunology.先天免疫处于心理神经免疫学的前沿。
Brain Behav Immun. 2004 Jan;18(1):1-6. doi: 10.1016/j.bbi.2003.09.008.

中枢胰岛素样生长因子-I可阻断功能性55kD肿瘤坏死因子受体小鼠中肿瘤坏死因子α诱导的疾病行为。

TNFalpha-induced sickness behavior in mice with functional 55 kD TNF receptors is blocked by central IGF-I.

作者信息

Palin Karine, Bluthé Rose-Marie, McCusker Robert H, Moos Françoise, Dantzer Robert, Kelley Keith W

机构信息

Department of Animal Sciences, Integrative Immunology and Behavior Program, Laboratory of Integrative Immunophysiology, University of Illinois at Urbana--Champaign, IL, USA.

出版信息

J Neuroimmunol. 2007 Jul;187(1-2):55-60. doi: 10.1016/j.jneuroim.2007.04.011. Epub 2007 May 18.

DOI:10.1016/j.jneuroim.2007.04.011
PMID:17512609
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2915825/
Abstract

A variety of pathogenic insults cause synthesis of tumor necrosis factor (TNF)alpha in the brain, resulting in sickness behavior. Here we used TNF-receptor (TNF-R)2-deficient and wild-type mice to demonstrate that the reduction in social exploration of a novel juvenile, the increase in immobility and the loss of body weight caused by central TNFalpha (i.c.v., 50 ng/mouse) are blocked by central pre-treatment with the multifunctional peptide, insulin-like growth factor (IGF-I; i.c.v., 300 ng/mouse). These results establish that sickness behavior induced by central TNFalpha via the TNF-R1 (p55) is directly opposed by IGF-I in the brain.

摘要

多种致病性损伤会导致大脑中肿瘤坏死因子（TNF）α的合成，从而引发疾病行为。在此，我们使用肿瘤坏死因子受体（TNF-R）2缺陷型和野生型小鼠来证明，中枢注射TNFα（脑室内注射，50 ng/只小鼠）所导致的对陌生幼鼠社交探索行为的减少、不动时间的增加以及体重的减轻，可被多功能肽胰岛素样生长因子（IGF-I；脑室内注射，300 ng/只小鼠）的中枢预处理所阻断。这些结果表明，中枢TNFα通过TNF-R1（p55）诱导的疾病行为在大脑中直接受到IGF-I的对抗。