Evidence map›Paper›PMID 30798405›Full record

ArticlePsychopharmacology2019

Environmental enrichment improves pain sensitivity, depression-like phenotype, and memory deficit in mice with neuropathic pain: role of NPAS4.

Xing-Ming Wang, Guang-Fen Zhang, Min Jia, Ze-Min Xie, Jian-Jun Yang, Jin-Chun Shen, Zhi-Qiang Zhou

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Psychopharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

19 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Mechanisms of comorbidity between Alzheimer's disease and pain.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
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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

7 authors at 4 institutions in 1 country.

Xing-Ming WangDepartment of Anesthesiology, Zhongda Hospital, Medical School, Southeast University, Nanjing, 210029, China.
Guang-Fen ZhangDepartment of Anesthesiology, Zhongda Hospital, Medical School, Southeast University, Nanjing, 210029, China.
Min JiaDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, 210002, China.
Ze-Min XieDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, 210002, China.
Jian-Jun YangDepartment of Anesthesiology, The first affiliated hospital of Zhengzhou University, Zhengzhou, 450052, China.
Jin-Chun ShenDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, 210002, China. yyshen0203@163.com.
Zhi-Qiang ZhouDepartment of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing, 210002, China. zq_zhou@163.com.
Nanjing General Hospital of Nanjing Military Command · CNNanjing University · CNZhongda Hospital Southeast University · CNFirst Affiliated Hospital of Zhengzhou University · CN

Funding

National Natural Science Foundation of China 81471105National Natural Science Foundation of China 81571083
6 · The paper itself

Abstract

Patients suffering from neuropathic pain have a higher incidence of depression and cognitive decline. Although environment enrichment (EE) may be effective in the treatment of neuropathic pain, the precise mechanisms underlying its actions remain determined. The aim of the study was to examine the molecular mechanisms underlying the EE's beneficial effects in mice with neuropathic pain. EE attenuated the pain threshold reduction, depression-like phenotype, and memory deficit in mice after chronic constriction injury (CCI). Furthermore, EE attenuated decreased neurogenesis and increased inflammation in the hippocampus of mice with neuropathic pain after CCI. Moreover, the suppression of adult hippocampal neurogenesis by temozolomide antagonized the beneficial effects of EE on depression-like phenotype and cognitive deficit in the mice with neuropathic pain. In addition, lipopolysaccharide-induced increase in tumor necrosis factor-α (TNF-α) in the hippocampus antagonized the beneficial effects of EE for these behavioral abnormalities in mice with neuropathic pain. Knock-down of NPAS4 (neuronal PAS domain protein 4) in the hippocampus by lentivirus targeting NPAS4 blocked these beneficial effects of EE in the mice with neuropathic pain. These all findings suggest that hippocampal NPAS4 plays a key role in the beneficial effects of EE on the pain sensitivity, depression-like phenotype, and memory deficit in mice with neuropathic pain. Therefore, it is likely that NPAS4 would be a new therapeutic target for perceptional, affective, and cognitive dimensions in patients with chronic pain.

Indexed as

EnvironmentAnimalsBasic Helix-Loop-Helix ProteinsDepressionHippocampusMaleMemory DisordersMiceMice, Inbred C57BLNeuralgiaNeurogenesisPain ThresholdPhenotypeTemozolomideBasic Helix-Loop-Helix ProteinsNpas4 protein, mouseTemozolomideCognitionDepressionInflammationNeurogenesisNeuropathicNpas4

Identifiers

PMID30798405
OpenAlexW2916873888

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.