Evidence map›Paper›PMID 29623029›Full record

ArticleFrontiers in molecular neuroscience2018

Hypersensitivity of Prelimbic Cortex Neurons Contributes to Aggravated Nociceptive Responses in Rats With Experience of Chronic Inflammatory Pain.

Xiao-Cen Fan, Su Fu, Feng-Yu Liu, Shuang Cui, Ming Yi, You Wan

Open access · goldAbstract read
In one paragraph

Article in Frontiers in molecular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Targeting 5-HTNeuroscience letters · 2022
    Article
  6. Review
  7. Review
  8. Neocortical circuits in pain and pain relief.Nature reviews. Neuroscience · 2021
    Review
  9. The role of medial prefrontal cortex projections to locus ceruleus in mediating the sex differences in behavior in mice with inflammatory pain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  10. Article
  11. Article
  12. Article
  13. The transition to compulsion in addiction.Nature reviews. Neuroscience · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review
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

6 authors at 2 institutions in 1 country.

Xiao-Cen FanNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Su FuNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Feng-Yu LiuNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Shuang CuiNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Ming YiNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, China.
You WanNeuroscience Research Institute and Department of Neurobiology, School of Basic Medical Sciences, Peking University, Beijing, China.
Peking University · CNNational Health and Family Planning Commission · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous experience of chronic pain causes enhanced responses to upcoming noxious events in both humans and animals, but the underlying mechanisms remain unclear. In the present study, we found that rats with complete Freund's adjuvant (CFA)-induced chronic inflammatory pain experience exhibited aggravated pain responses to later formalin test. Enhanced neuronal activation upon formalin assaults and increased phosphorylated cAMP-response element binding protein (CREB) were observed in the prelimbic cortex (PL) of rats with chronic inflammatory pain experience, and inhibiting PL neuronal activities reversed the aggravated pain. Inflammatory pain experience induced persistent p38 mitogen-activated protein kinase (MAPK; p38) but not extracellular regulated protein kinase (ERK) or c-Jun N-terminal kinase (JNK) hyperphosphorylation in the PL. Inhibiting the p38 phosphorylation in PL reversed the aggravated nociceptive responses to formalin test and down-regulated enhanced phosphorylated CREB in the PL. Chemogenetics identified PL-periaqueductal gray (PAG) but not PL-nucleus accumbens (NAc) as a key pathway in inducing the aggravated formalin pain. Our results demonstrate that persistent hyperphosphorylation of p38 in the PL underlies aggravated nociceptive responses in rats with chronic inflammatory pain experience.

Indexed as

chronic painp38painprefrontal cortexprelimbic cortex

Identifiers

PMID29623029
PMCPMC5874315
OpenAlexW2793011695

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.