TNFR1 absence protects against memory deficit induced by sepsis possibly through over-expression of hippocampal BDNF (vol 30, pg 669, 2015)

被引：3

作者：

Calsavara, Allan C. ^{[1
,2
]}

Soriani, Frederico M. ^{[3
]}

Vieira, Leda Q. ^{[3
]}

Costa, Priscila A. ^{[1
]}

Rachid, Milene A. ^{[3
]}

Teixeira, Antnio L. ^{[1
]}

机构：

[1] Univ Fed Minas Gerais, Sch Med, Interdisciplinary Lab Med Invest, Belo Horizonte, MG, Brazil

[2] Univ Fed Ouro Preto, Sch Med, Ouro Preto, MG, Brazil

[3] Univ Fed Minas Gerais, Inst Biol Sci, Belo Horizonte, MG, Brazil

来源：

METABOLIC BRAIN DISEASE | 2015年 / 30卷 / 03期

关键词：

Sepsis; Memory impairment; TNFR1; TNF; BDNF;

D O I：

10.1007/s11011-014-9620-6

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

The involvement of TNF-alpha type 1 receptor (TNFR1) in memory deficits induced by sepsis was explored by using TNFR1 knockout (KO) mice. We reported that wild type (WT) mice presented memory deficits in the novel object recognition test 10 days after sepsis induced by cecum ligation and perforation (CLP). These deficits were not observed in TNFR1 KO mice. The involvement of serum and brain cytokines TNF-alpha, IL-1 beta, IL-6, IFN-gamma and IL-10 was then investigated. TNFR1 KO mice had higher serum levels of TNF-alpha and IL-1 beta, and brain levels of TNF-alpha than WT mice. After CLP, the brain levels of TNF-alpha, IL-1 beta, IL-6 and IFN-gamma increased in both WT and KO mice. Our next step was to determine the expression of inflammatory cytokines, BDNF and TrKb in the hippocampus. The absence of TNFR1 in mice subjected to polymicrobial sepsis resulted in higher BDNF expression in the hippocampus. In conclusion, after CLP, memory is preserved in the absence of TNFR1. This finding was associated with increased BDNF expression in the hippocampus.

引用

页码：679 / 679

页数：1