Evidence map›Paper›PMID 26650043›Full record

ArticleMolecular neurobiology2016

NOX2 Mediated-Parvalbumin Interneuron Loss Might Contribute to Anxiety-Like and Enhanced Fear Learning Behavior in a Rat Model of Post-Traumatic Stress Disorder.

Fang-Fang Liu, Lin-Dong Yang, Xiao-Ru Sun, Hui Zhang, Wei Pan, Xing-Ming Wang, Jian-Jun Yang, Mu-Huo Ji, Hong-Mei Yuan

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 22% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.

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  15. Opposed hemodynamic responses following increased excitation and parvalbumin-based inhibition.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 1 country.

Fang-Fang LiuDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Lin-Dong YangDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Xiao-Ru SunDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Hui ZhangDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Wei PanDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Xing-Ming WangDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Jian-Jun YangDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China.
Mu-Huo JiDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, China. jimuhuo2009@sina.com.
Hong-Mei YuanDepartment of Anesthesiology, Nanjing Maternity and Child Health Care Hospital, Nanjing Medical University, Nanjing, China. Yuanhm667@126.com.
Nanjing University · CNNanjing General Hospital of Nanjing Military Command · CNJiangsu Province Hospital · CNNanjing Maternity and Child Health Care Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Post-traumatic stress disorder (PTSD) is a common psychiatric disease following exposure to a severe traumatic event or physiological stress, yet the precise mechanisms underlying PTSD remains largely to be determined. Using an animal model of PTSD induced by a single prolonged stress (SPS), we assessed the role of hippocampal nicotinamide adenosine dinucleotide phosphate (NADPH) oxidase 2 (NOX2) and parvalbumin (PV) interneurons in the development of PTSD symptoms. In the present study, behavioral tests were performed by the open field (day 13 after SPS) and fear conditioning tests (days 13 and 14 after SPS). For the interventional study, rats were chronically treated with a NADPH oxidase inhibitor apocynin either by early or delayed administration. The levels of tumor necrosis factor-alpha, interleukin (IL)-1β, IL-6, IL-10, malondialdehyde, superoxide dismutase, NOX2, 4-hydroxynonenal, and PV in the hippocampus were measured at the indicated time points. In the present study, we showed that SPS rats displayed anxiety-like and enhanced fear learning behavior, which was accompanied by the increased expressions of malondialdehyde, IL-6, NOX2, 4-hydroxynonenal, and decreased PV expression. Notably, early but not delayed treatment with apocynin reversed all these abnormalities after SPS. In conclusion, our results provided evidence that NOX2 activation in the hippocampus, at least in part, contributes to oxidative stress and neuroinflammation, which further results in PV interneuron loss and consequent PTSD symptoms in a rat model of PTSD induced by SPS.

Indexed as

Behavior, AnimalFearLearningAcetophenonesAldehydesAnimalsAnxietyDisease Models, AnimalHippocampusInterleukin-6InterneuronsMaleMalondialdehydeNADPH Oxidase 2ParvalbuminsRats, Sprague-Dawley4-hydroxy-2-nonenalAcetophenonesacetovanilloneAldehydesCybb protein, ratInterleukin-6MalondialdehydeNADPH Oxidase 2ParvalbuminsAnxietyFear learningNADPHPVSingle prolonged stress

Identifiers

PMID26650043
OpenAlexW2290496828

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.