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Sepsis-induced selective parvalbumin interneuron phenotype loss and cognitive impairments may be mediated by NADPH oxidase 2 activation in mice

Overview of attention for article published in Journal of Neuroinflammation, January 2015
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Title
Sepsis-induced selective parvalbumin interneuron phenotype loss and cognitive impairments may be mediated by NADPH oxidase 2 activation in mice
Published in
Journal of Neuroinflammation, January 2015
DOI 10.1186/s12974-015-0401-x
Pubmed ID
Authors

Mu-Huo Ji, Li-Li Qiu, Hui Tang, Ling-Sha Ju, Xiao-Ru Sun, Hui Zhang, Min Jia, Zhi-Yi Zuo, Jin-Chun Shen, Jian-Jun Yang, Ji, Mu-Huo, Qiu, Li-Li, Tang, Hui, Ju, Ling-Sha, Sun, Xiao-Ru, Zhang, Hui, Jia, Min, Zuo, Zhi-Yi, Shen, Jin-Chun, Yang, Jian-Jun

Abstract

Sepsis-associated encephalopathy (SAE) is a diffuse brain dysfunction caused by many pathological events, including neuroinflammation and oxidative stress damage. Increasing evidence suggests that parvalbumin (PV) interneurons play a key role in the cognitive process, whereas the dysfunction of these interneurons has been implicated in a number of major psychiatric disorders. Here, we aimed to investigate whether enhanced inflammation and oxidative stress-mediated PV interneuron phenotype loss plays a role in sepsis-induced cognitive impairments. Male C57BL/6 mice were subjected to cecal ligation and puncture or sham operation. For the interventional study, the animals were chronically treated with a nicotinamide adenine dinucleotide phosphate (NADPH) oxidase inhibitor, apocynin, at 5 mg/kg. The mice were euthanized at the indicated time points, and the brain tissues were harvested for determination of the PV, membrane subunit of NADPH oxidase gp91(phox), and markers of oxidative stress (4-hydroxynonenal and malondialdehyde) and inflammation (tumor necrosis factor alpha (TNF-α), interleukin (IL)-1β, IL-6, and IL-10). A separate cohort of animals was used to evaluate the behavioral alterations by the open field and fear conditioning tests. Primary hippocampal neuronal cultures were used to investigate the mechanisms underlying the dysfunction of PV interneurons. Sepsis resulted in cognitive impairments, which was accompanied by selective phenotype loss of PV interneurons and increased gp91(phox), 4-hydroxynonenal, malondialdehyde, IL-1β, and IL-6 expressions. Notably, these abnormalities could be rescued by apocynin treatment. Selective phenotype loss of PV interneurons, as a result of NADPH oxidase 2 (Nox2) activation, might partly contribute to cognitive impairments in a mouse model of SAE.

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Mendeley readers

The data shown below were compiled from readership statistics for 53 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 53 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 11 21%
Researcher 8 15%
Student > Doctoral Student 6 11%
Student > Postgraduate 5 9%
Student > Master 5 9%
Other 9 17%
Unknown 9 17%
Readers by discipline Count As %
Neuroscience 14 26%
Medicine and Dentistry 10 19%
Agricultural and Biological Sciences 7 13%
Biochemistry, Genetics and Molecular Biology 4 8%
Psychology 3 6%
Other 4 8%
Unknown 11 21%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 22 June 2016.
All research outputs
#10,132,567
of 11,426,369 outputs
Outputs from Journal of Neuroinflammation
#1,096
of 1,290 outputs
Outputs of similar age
#199,241
of 243,584 outputs
Outputs of similar age from Journal of Neuroinflammation
#45
of 49 outputs
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