Evidence map›Paper›PMID 15169847›Full record

ArticleThe Journal of physiology2004

Isoflurane depresses glutamate release by reducing neuronal excitability at the Drosophila neuromuscular junction.

David J Sandstrom

Open access · greenAbstract read
In one paragraph

Article in The Journal of physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.9field-weighted citation impact, top 33% 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, 63 citations in OpenAlex.

  1. Article
  2. Review
  3. Opposed hemodynamic responses following increased excitation and parvalbumin-based inhibition.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021
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  16. Anesthesia and the quantitative evaluation of neurovascular coupling.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012
    Review
  17. Article
  18. Article
  19. Article
  20. The RhoGAP crossveinless-c interacts with Dystrophin and is required for synaptic homeostasis at the Drosophila neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
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

1 author at 1 institution in 1 country.

David J SandstromLaboratory of Molecular Biology, National Institute of Mental Health, National Institutes of Health MSC 4034, Bethesda, MD 20892, USA. sandstrd@mail.nih.gov
National Institutes of Health · US

Funding

Genetic Neurobiology Of DrosophilaZIAMH002228 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI WHITE, BENJAMIN H · 2009 to 2013
$4.8M
GENETIC NEUROBIOLOGY OF DROSOPHILAZ01MH002228 · NIMH · NATIONAL INSTITUTE OF MENTAL HEALTH · PI NASH, HOWARD A · 1986 to 2008
$4.1M
6 · The paper itself

Abstract

The mechanisms through which volatile general anaesthetics exert their behavioural effects remain unclear. The accessibility of the Drosophila larval neuromuscular junction to genetic and neurophysiological analysis has made it an attractive model system for identification of anaesthetic targets. This study provides a mechanistic basis for the genetic analysis of anaesthetic action, by analysing the neurophysiological effects of the volatile anaesthetic isoflurane on axonal and synaptic function in the Drosophila larva. The most robust effect of isoflurane was a reversible decrease in the amplitude and area of glutamatergic excitatory junctional currents (EJCs) evoked at the neuromuscular junction. Isoflurane did not affect postsynaptic glutamate receptor function detectably, in that the amplitudes, areas and decay times of spontaneous miniature EJCs were unchanged at any concentration. Therefore, decreased EJC amplitude resulted from reduction of neurotransmitter release. Reduced neurotransmitter release was associated with decreased presynaptic excitability, measured as increased delay to EJC onset and reduced axonal conduction velocity. EJC amplitude was rescued to control levels by direct electrotonic stimulation of the synapse in the presence of tetrodotoxin, indicating that isoflurane inhibits neurotransmitter release by reducing presynaptic excitability. In addition, isoflurane reduced release probability, measured as increased paired-pulse facilitation. The EC(50) for suppression of larval locomotion was similar to that for reduction of transmitter release, indicating that the axonal and synaptic effects were occurring in a behaviourally relevant range. These results provide a cellular context for ongoing genetic and neurophysiological analyses of volatile anaesthetic action in Drosophila, and suggest candidate anaesthetic target molecules.

Indexed as

Anesthetics, InhalationAnimalsAxonsDrosophilaGlutamic AcidIsofluraneLarvaMotor NeuronsNeuromuscular JunctionSynaptic TransmissionAnesthetics, InhalationGlutamic AcidIsoflurane

Identifiers

PMID15169847
PMCPMC1664974
OpenAlexW2140551697

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.