Evidence map›Paper›PMID 27229176›Full record

ArticleScientific reports2016

Ciguatoxin reduces regenerative capacity of axotomized peripheral neurons and delays functional recovery in pre-exposed mice after peripheral nerve injury.

Ngan Pan Bennett Au, Gajendra Kumar, Pallavi Asthana, Chung Tin, Yim Ling Mak, Leo Lai Chan, Paul Kwan Sing Lam, Chi Him Eddie Ma

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.4field-weighted citation impact, top 14% 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

17 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. A small molecule M1 promotes optic nerve regeneration to restore target-specific neural activity and visual function.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Cyanobacteria, Cyanotoxins, and Neurodegenerative Diseases:International journal of molecular sciences · 2021
    Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Article
  17. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 2 countries.

Ngan Pan Bennett AuDepartment of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Gajendra KumarDepartment of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Pallavi AsthanaDepartment of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Chung TinDepartment of Mechanical and Biomedical Engineering, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Yim Ling MakState Key Laboratory in Marine Pollution, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Leo Lai ChanDepartment of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Paul Kwan Sing LamState Key Laboratory in Marine Pollution, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
Chi Him Eddie MaDepartment of Biomedical Sciences, City University of Hong Kong, Tat Chee Avenue, Hong Kong.
City University of Hong Kong · HKCity University of Hong Kong, Shenzhen Research Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ciguatera fish poisoning (CFP) results from consumption of tropical reef fish containing ciguatoxins (CTXs). Pacific (P)-CTX-1 is among the most potent known CTXs and the predominant source of CFP in the endemic region responsible for the majority of neurological symptoms in patients. Chronic and persistent neurological symptoms occur in some CFP patients, which often result in incomplete functional recovery for years. However, the direct effects of exposure to CTXs remain largely unknown. In present study, we exposed mice to CTX purified from ciguatera fish sourced from the Pacific region. P-CTX-1 was detected in peripheral nerves within hours and persisted for two months after exposure. P-CTX-1 inhibited axonal regrowth from axotomized peripheral neurons in culture. P-CTX-1 exposure reduced motor function in mice within the first two weeks of exposure before returning to baseline levels. These pre-exposed animals exhibited delayed sensory and motor functional recovery, and irreversible motor deficits after peripheral nerve injury in which formation of functional synapses was impaired. These findings are consistent with reduced muscle function, as assessed by electromyography recordings. Our study provides strong evidence that the persistence of P-CTX-1 in peripheral nerves reduces the intrinsic growth capacity of peripheral neurons, resulting in delayed functional recovery after injury.

Indexed as

AnimalsAxotomyCells, CulturedCell SurvivalCiguatoxinsGanglia, SpinalMaleMice, Inbred C57BLMovementNerve RegenerationNeuronal OutgrowthNeuronsPeripheral Nerve InjuriesPoisonsRecovery of FunctionCiguatoxinsPoisons

Identifiers

PMID27229176
PMCPMC4882531
OpenAlexW2399679346

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.