Evidence map›Paper›PMID 21289602›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2011

Peripheral nerve injury leads to working memory deficits and dysfunction of the hippocampus by upregulation of TNF-α in rodents.

Wen-Jie Ren, Yong Liu, Li-Jun Zhou, Wei Li, Yi Zhong, Rui-Ping Pang, Wen-Jun Xin, Xu-Hong Wei, Jun Wang, He-Quan Zhu and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 117 papers.

0numbers the graph read from it
0cells of the map it votes in
117citing papers in PubMed
7.4field-weighted citation impact, top 2% 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

117 citing papers in PubMed, 233 citations in OpenAlex.

  1. Interleukin-1β Alters Hebbian Synaptic Plasticity in Multiple Sclerosis.International journal of molecular sciences · 2020
    Trial
  2. Trial
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Article

57 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 1 country.

Wen-Jie RenDepartment of Physiology, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, China.
Yong Liu
Li-Jun Zhou
Wei Li
Yi Zhong
Rui-Ping Pang
Wen-Jun Xin
Xu-Hong Wei
Jun Wang
He-Quan Zhu
Chang-You Wu
Zhi-Hai Qin
Guosong Liu
Xian-Guo Liu
Sun Yat-sen University · CNTsinghua University · CNInstitute of Biophysics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Patients with chronic pain usually suffer from working memory deficits, which may decrease their intellectual ability significantly. Despite intensive clinical studies, the mechanism underlying this form of memory impairment remains elusive. In this study, we investigated this issue in the spared nerve injury (SNI) model of neuropathic pain, a most common form of chronic pain. We found that SNI impaired working memory and short-term memory in rats and mice. To explore the potential mechanisms, we studied synaptic transmission/plasticity in hippocampus, a brain region critically involved in memory function. We found that frequency facilitation, a presynaptic form of short-term plasticity, and long-term potentiation at CA3-CA1 synapses were impaired after SNI. Structurally, density of presynaptic boutons in hippocampal CA1 synapses was reduced significantly. At the molecular level, we found that tumor necrosis factor-α (TNF-α) increased in cerebrospinal fluid, in hippocampal tissue and in plasma after SNI. Intracerebroventricular or intrahippocampal injection of recombinant rat TNF mimicked the effects of SNI in naive rats, whereas inhibition of TNF-α or genetic deletion of TNF receptor 1 prevented both memory deficits and synaptic dysfunction induced by SNI. As TNF-α is critical for development of neuropathic pain, we suggested that the over-production of TNF-α following peripheral nerve injury might lead to neuropathic pain and memory deficits, simultaneously.

Indexed as

Peripheral Nervous System DiseasesAnimalsDisease Models, AnimalElectric StimulationExcitatory Postsynaptic PotentialsHippocampusHyperalgesiaImmunosuppressive AgentsLong-Term PotentiationMaleMaze LearningMemory DisordersMemory, Short-TermMiceMice, KnockoutPresynaptic TerminalsImmunosuppressive AgentsReceptors, Tumor Necrosis Factor, Type IRNA, MessengerThalidomideTumor Necrosis Factor-alpha

Identifiers

PMID21289602
PMCPMC3077267
OpenAlexW2038211748

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.