Evidence map›Paper›PMID 29422839›Full record

ArticleFrontiers in cellular neuroscience2018

Exercise-Induced Fatigue Impairs Bidirectional Corticostriatal Synaptic Plasticity.

Jing Ma, Huimin Chen, Xiaoli Liu, Lingtao Zhang, Decai Qiao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Brain plasticity and ginseng.Journal of ginseng research · 2024
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Application of traditional Chinese therapy in sports medicine.Sports medicine and health science · 2021
    Review
  13. Antioxidants (Basel, Switzerland) · 2020
    Article
  14. Article
  15. Effects of Exercise on Long-Term Potentiation in Neuropsychiatric Disorders.Advances in experimental medicine and biology · 2020
    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

5 authors at 1 institution in 1 country.

Jing MaCollege of Physical Education and Sports, Beijing Normal University, Beijing, China.
Huimin ChenCollege of Physical Education and Sports, Beijing Normal University, Beijing, China.
Xiaoli LiuCollege of Physical Education and Sports, Beijing Normal University, Beijing, China.
Lingtao ZhangCollege of Physical Education and Sports, Beijing Normal University, Beijing, China.
Decai QiaoCollege of Physical Education and Sports, Beijing Normal University, Beijing, China.
Beijing Normal University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exercise-induced fatigue (EF) is a ubiquitous phenomenon in sports competition and training. It can impair athletes' motor skill execution and cognition. Corticostriatal synaptic plasticity is considered to be the cellular mechanism of movement control and motor learning. However, the effect of EF on corticostriatal synaptic plasticity remains elusive. In the present study, using field excitatory postsynaptic potential recording, we found that the corticostriatal long-term potentiation (LTP) and long-term depression (LTD) were both impaired in EF mice. To further investigate the cellular mechanisms underlying the impaired synaptic plasticity in corticostriatal pathway, whole-cell patch clamp recordings were carried out on striatal medium spiny neurons (MSNs). MSNs in EF mice exhibited increased spontaneous excitatory postsynaptic current (sEPSC) frequency and decreased paired-pulse ratio (PPR), while with normal basic electrophysiological properties and normal sEPSC amplitude. Furthermore, the N-methyl-D-aspartate (NMDA)/α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) ratio of MSNs was reduced in EF mice. These results suggest that the enhanced presynaptic glutamate (Glu) release and downregulated postsynaptic NMDA receptor function lead to the impaired corticostriatal plasticity in EF mice. Taken together, our findings for the first time show that the bidirectional corticostriatal synaptic plasticity is impaired after EF, and suggest that the aberrant corticostriatal synaptic plasticity may be involved in the production and/or maintenance of EF.

Indexed as

corticostriatal pathwayexercise-induced fatigueglutamate releaselong-term depressionlong-term potentiation

Identifiers

PMID29422839
PMCPMC5788965
OpenAlexW2791376485

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.