Evidence map›Paper›PMID 11404407›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Drosophila alpha- and beta-spectrin mutations disrupt presynaptic neurotransmitter release.

D E Featherstone, W S Davis, R R Dubreuil, K Broadie

Open access · hybridAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. 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
1.7field-weighted citation impact, top 18% 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, 97 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Tissue-type plasminogen activator triggers the synaptic vesicle cycle in cerebral cortical neurons.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2015
    Article
  13. Inositol Hexakisphosphate Kinase-3 Regulates the Morphology and Synapse Formation of Cerebellar Purkinje Cells via Spectrin/Adducin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  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 2 institutions in 1 country.

D E FeatherstoneDepartment of Biology, University of Utah, Salt Lake City, Utah 84112-0840, USA.
W S Davis
R R Dubreuil
K Broadie
University of Utah · USUniversity of Chicago · US

Funding

GENETIC ANALYSIS OF SYNAPSE FORMATION AND FUNCTIONR01GM054544 · NIGMS · VANDERBILT UNIVERSITY · PI BROADIE, KENDAL · 1997 to 2010
$2.9M
GENETIC STUDIES OF THE MEMBRANE SKELETONR01GM049301 · NIGMS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI DUBREUIL, RONALD R · 1995 to 2004
$1.1M
NIGMS NIH HHS GM49301NIGMS NIH HHS GM54544NIGMS NIH HHS R01 GM049301NIGMS NIH HHS R01 GM054544
6 · The paper itself

Abstract

Spectrins are plasma membrane-associated cytoskeletal proteins implicated in several aspects of synaptic development and function, including presynaptic vesicle tethering and postsynaptic receptor aggregation. To test these hypotheses, we characterized Drosophila mutants lacking either alpha- or beta-spectrin. The Drosophila genome contains only one alpha-spectrin and one conventional beta-spectrin gene, making it an ideal system to genetically manipulate spectrin levels and examine the resulting synaptic alterations. Both spectrin proteins are strongly expressed in the Drosophila neuromusculature and highly enriched at the glutamatergic neuromuscular junction. Protein null alpha- and beta-spectrin mutants are embryonic lethal and display severely disrupted neurotransmission without altered morphological synaptogenesis. Contrary to current models, the absence of spectrins does not alter postsynaptic glutamate receptor field function or the ultrastructural localization of presynaptic vesicles. However, the subcellular localization of numerous synaptic proteins is disrupted, suggesting that the defects in presynaptic neurotransmitter release may be attributable to inappropriate assembly, transport, or localization of proteins required for synaptic function.

Indexed as

Calcium-Binding ProteinsAnimalsDrosophilaEmbryo, NonmammalianGenes, LethalGlutamic AcidImmunohistochemistryIn Vitro TechniquesLarvaMembrane GlycoproteinsMembrane ProteinsMutationNerve Tissue ProteinsNeuromuscular JunctionNeurotransmitter AgentsPatch-Clamp TechniquesCalcium-Binding ProteinsGlutamic AcidMembrane GlycoproteinsMembrane ProteinsNerve Tissue ProteinsNeurotransmitter AgentsQa-SNARE ProteinsSpectrinSynapsinsSynaptotagmins

Identifiers

PMID11404407
PMCPMC6762771
OpenAlexW1593633620

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.