Evidence map›Paper›PMID 28123433›Full record

ReviewNeural regeneration research2016

Cortical spreading depression-induced preconditioning in the brain.

Ping-Ping Shen, Shuai Hou, Di Ma, Ming-Ming Zhao, Ming-Qin Zhu, Jing-Dian Zhang, Liang-Shu Feng, Li Cui, Jia-Chun Feng

Open access · goldAbstract readReview
In one paragraph

Review in Neural regeneration research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

13 citing papers in PubMed, 26 citations in OpenAlex.

  1. Review
  2. The NMDA receptor antagonists memantine and ketamine as anti-migraine agents.Naunyn-Schmiedeberg's archives of pharmacology · 2023
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  8. Review
  9. The physiology of regulated BDNF release.Cell and tissue research · 2020
    Review
  10. Review
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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 2 institutions in 1 country.

Ping-Ping ShenInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Shuai HouInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Di MaInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Ming-Ming ZhaoInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Ming-Qin ZhuInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Jing-Dian ZhangInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Liang-Shu FengInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Li CuiInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.
Jia-Chun FengInstitute of Neuroscience Center and Neurology Department, the First Affiliated Hospital of Jilin University, Changchun, Jilin Province, China.ORCID 0000-0002-5999-2492
Jilin University · CNFirst Hospital of Jilin University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cortical spreading depression is a technique used to depolarize neurons. During focal or global ischemia, cortical spreading depression-induced preconditioning can enhance tolerance of further injury. However, the underlying mechanism for this phenomenon remains relatively unclear. To date, numerous issues exist regarding the experimental model used to precondition the brain with cortical spreading depression, such as the administration route, concentration of potassium chloride, induction time, duration of the protection provided by the treatment, the regional distribution of the protective effect, and the types of neurons responsible for the greater tolerance. In this review, we focus on the mechanisms underlying cortical spreading depression-induced tolerance in the brain, considering excitatory neurotransmission and metabolism, nitric oxide, genomic reprogramming, inflammation, neurotropic factors, and cellular stress response. Specifically, we clarify the procedures and detailed information regarding cortical spreading depression-induced preconditioning and build a foundation for more comprehensive investigations in the field of neural regeneration and clinical application in the future.

Indexed as

cellular stress responsecortical spreading depressionexcitatory neurotransmissiongenomic reprogramminginflammationischemic tolerancenerve regenerationneural regenerationneuronal depolarizationneurotropic factorsnitric oxideperi-infarct depolarization

Identifiers

PMID28123433
PMCPMC5204245
OpenAlexW2565086550

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.