Evidence map›Paper›PMID 8656281›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1996

Homeostasis of synaptic transmission in Drosophila with genetically altered nerve terminal morphology.

B A Stewart, C M Schuster, C S Goodman, H L Atwood

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

47 citing papers in PubMed, 158 citations in OpenAlex.

  1. Article
  2. Activity-Dependent Global Downscaling of Evoked Neurotransmitter Release across Glutamatergic Inputs inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
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  9. Review
  10. Heat shock response and homeostatic plasticity.Frontiers in cellular neuroscience · 2015
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  14. Article
  15. Retrograde bone morphogenetic protein signaling shapes a key circadian pacemaker circuit.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  16. Article
  17. Regulation of Fasciclin II and synaptic terminal development by the splicing factor beag.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  18. Review
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

B A StewartDepartment of Physiology, University of Toronto, Ontario, Canada.
C M Schuster
C S Goodman
H L Atwood
University of Toronto · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We present a new test of the hypothesis that synaptic strength is directly related to nerve terminal morphology through analysis of synaptic transmission at Drosophila neuromuscular junctions with a genetically reduced number of nerve terminal varicosities. Synaptic transmission would decrease in target cells with fewer varicosities if there is a relationship between the number of varicosities and the strength of synaptic transmission. Animals that have an extreme hypomorphic allele of the gene for the cell adhesion molecule Fasciclin II possess fewer synapse-bearing nerve terminal varicosities; nevertheless, synaptic strength is maintained at a normal level for the muscle cell as a whole. Fewer failures of neurotransmitter release and larger excitatory junction potentials from individual varicosities, as well as more frequent spontaneous release and larger quantal units, provide evidence for enhancement of transmitter release from varicosities in the mutant. Ultrastructural analysis reveals that mutant nerve terminals have bigger synapses with more active zones per synapse, indicating that synaptic enlargement and an accompanying increase in synaptic complexity provide for more transmitter release at mutant varicosities. These results show that morphological parameters of transmitting nerve terminals can be adjusted to functionally compensate for genetic perturbations, thereby maintaining optimal synaptic transmission.

Indexed as

AnimalsCell Adhesion Molecules, NeuronalDrosophilaHomeostasisMicroscopy, ElectronMusclesMutationNerve FibersNeuromuscular JunctionPresynaptic TerminalsSynapsesSynaptic TransmissionCell Adhesion Molecules, Neuronalfasciclin II

Identifiers

PMID8656281
PMCPMC6578607
OpenAlexW2106349285

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.