Evidence map›Paper›PMID 27784805›Full record

ArticleJournal of neurophysiology2017

The acute inhibition of enteric glial metabolism with fluoroacetate alters calcium signaling, hemichannel function, and the expression of key proteins.

Jonathon L McClain, Brian D Gulbransen

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed, 36 citations in OpenAlex.

  1. Purinergic P2YPurinergic signalling · 2025
    Article
  2. Article
  3. Voltage-gated potassium channels control extended access cocaine seeking: a role for nucleus accumbens astrocytes.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2024
    Article
  4. Article
  5. Article
  6. BQ788 reveals glial ETBritish journal of pharmacology · 2023
    Article
  7. Article
  8. Functional Intraregional and Interregional Heterogeneity between Myenteric Glial Cells of the Colon and Duodenum in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Circuit-specific enteric glia regulate intestinal motor neurocircuits.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  16. Influence ofNutrients · 2021
    Article
  17. Review
  18. Article
  19. Article
  20. Functional circuits and signal processing in the enteric nervous system.Cellular and molecular life sciences : CMLS · 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

2 authors at 1 institution in 1 country.

Jonathon L McClainDepartment of Physiology, Michigan State University, East Lansing, Michigan; and.
Brian D GulbransenDepartment of Physiology, Michigan State University, East Lansing, Michigan; and gulbrans@msu.edu.ORCID 0000-0003-1145-3227
Michigan State University · US

Funding

Role of enteric glia in the death of neurons during gut inflammationR01DK103723 · NIDDK · MICHIGAN STATE UNIVERSITY · PI BRIAN D. GULBRANSEN · 2015 to 2026
$4.7M
NIDDK NIH HHS R01 DK103723
6 · The paper itself

Abstract

Glia play key roles in the regulation of neurotransmission in the nervous system. Fluoroacetate (FA) is a metabolic poison widely used to study glial functions by disrupting the tricarboxylic acid cycle enzyme aconitase. Despite the widespread use of FA, the effects of FA on essential glial functions such as calcium (Ca NEW & NOTEWORTHY: Our study shows that the acute impairment of enteric glial metabolism with fluoroacetate (FA) alters specific glial functions that are associated with the modification of neurotransmission in the gut. These include subtle changes to glial agonist-evoked calcium signaling, the subsequent disruption of connexin-43 hemichannels, and changes in protein expression that are consistent with a transition to reactive glia. These changes in glial function offer a mechanistic explanation for the effects of FA on peripheral neuronal networks.

Indexed as

Adenosine DiphosphateAniline CompoundsAnimalsCalcium SignalingCell CountConnexin 43ELAV-Like Protein 3ELAV-Like Protein 4FemaleFluoroacetatesGene Expression RegulationGlial Fibrillary Acidic ProteinMaleMiceMice, Inbred C57BLMice, TransgenicAdenosine DiphosphateAniline CompoundsConnexin 43Elavl3 protein, mouseELAV-Like Protein 3ELAV-Like Protein 4Fluo 4FluoroacetatesGlial Fibrillary Acidic ProteinS100 Calcium Binding Protein beta SubunitSox10 protein, mouseSOXE Transcription FactorsXanthenesautonomic nervous systementeric glial cellsenteric nervous systemgliaintestine

Identifiers

PMID27784805
PMCPMC5236112
OpenAlexW2541400288

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.