Evidence map›Paper›PMID 21173083›Full record

ArticleThe Journal of physiology2011

Etomidate and propofol inhibit the neurotransmitter release machinery at different sites.

Bruce E Herring, Kyle McMillan, Carolyn M Pike, Jeremy Marks, Aaron P Fox, Zheng Xie

Erratum issuedOpen access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2011. 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 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 22% 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

26 citing papers in PubMed, 51 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Propofol decreases in vivo binding of 11C-PBR28 to translocator protein (18 kDa) in the human brain.Journal of nuclear medicine : official publication, Society of Nuclear Medicine · 2013
    Trial
  4. Review
  5. Synapse-Specific Trapping of SNARE Machinery Proteins in the AnesthetizedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
  6. Article
  7. Article
  8. Neural Ensemble Fragmentation in the AnesthetizedThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  9. Article
  10. Review
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

Bruce E HerringDepartment of Neurobiology, The University of Chicago, 5835 S. Cottage Grove Ave, Abbott Hall, Ab131, Chicago, IL 60637, USA.
Kyle McMillan
Carolyn M Pike
Jeremy Marks
Aaron P Fox
Zheng Xie
Pediatrics and Genetics · USUniversity of Chicago · US

Funding

Mechanisms of Co-Polymer-Mediated NeuroprotectionR01NS056313 · NINDS · UNIVERSITY OF CHICAGO · PI MARKS, JEREMY D · 2007 to 2011
$1.8M
Reversing anesthesia with CaffeineR01GM116119 · NIGMS · UNIVERSITY OF CHICAGO · PI FOX, AARON P. · 2015 to 2018
$1.2M
NIGMS NIH HHS R01 GM116119NINDS NIH HHS R01 NS056313
6 · The paper itself

Abstract

The mechanism of general anaesthetic action is only partially understood. Facilitation of inhibitory GABAA receptors plays an important role in the action of most anaesthetics, but is thought to be especially relevant in the case of intravenous anaesthetics, like etomidate and propofol. Recent evidence suggests that anaesthetics also inhibit excitatory synaptic transmission via a presynaptic mechanism(s), but it has been difficult to determine whether these agents act on the neurotransmitter release machinery itself. In the present study we sought to determine whether the intravenous anaesthetics propofol and etomidate inhibit the release machinery. For these studies we used an experimental approach that directly regulated [Ca2+]i at neurotransmitter release sites, thereby bypassing anaesthetic effects on channels and receptors in order to allow anaesthetic effects on the neurotransmitter release machinery to be examined in isolation. The data show that clinically relevant concentrations of propofol and etomidate inhibited the neurotransmitter release machinery in neurosecretory cells and in cultured hippocampal neurons. md130A is a mutant form of syntaxin with a truncated C-terminus. Overexpressing md130A in PC12 cells completely eliminated the reduction in neurotransmitter release produced by propofol, without affecting release itself. In contrast, overexpressing md130A in PC12 cells had little or no effect on the response to etomidate. These results suggest that both propofol and etomidate inhibit neurotransmitter release by a direct interaction with SNAREs and/or SNARE-associated proteins but they do so at different sites.

Indexed as

Anesthetics, IntravenousAnimalsBlotting, WesternCells, CulturedDose-Response Relationship, DrugEtomidateHippocampusNeuronsPatch-Clamp TechniquesPC12 CellsPropofolRatsRats, Sprague-DawleySynaptic TransmissionSynaptic VesiclesAnesthetics, IntravenousEtomidatePropofol

Identifiers

PMID21173083
PMCPMC3060590
OpenAlexW1594046881

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.