Evidence map›Paper›PMID 22500637›Full record

ArticleNeuron2012

Motorneurons require cysteine string protein-α to maintain the readily releasable vesicular pool and synaptic vesicle recycling.

José Luis Rozas, Leonardo Gómez-Sánchez, Josif Mircheski, Pedro Linares-Clemente, José Luis Nieto-González, M Eugenio Vázquez, Rafael Luján, Rafael Fernández-Chacón

Open access · bronzeAbstract read
PubMed Publisher
In one paragraph

Article in Neuron, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
4.1field-weighted citation impact, top 5% 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

46 citing papers in PubMed, 68 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Decoding transcriptomic signatures of cysteine string protein alpha-mediated synapse maintenance.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  5. Article
  6. NMJ-related diseases beyond the congenital myasthenic syndromes.Frontiers in cell and developmental biology · 2023
    Review
  7. Review
  8. Autophagy in the Neuronal Ceroid Lipofuscinoses (Batten Disease).Frontiers in cell and developmental biology · 2022
    Review
  9. Article
  10. AeLife · 2019
    Article
  11. Loss of postnatal quiescence of neural stem cells through mTOR activation upon genetic removal of cysteine string protein-α.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  12. Review
  13. GPCR regulation of secretion.Pharmacology & therapeutics · 2018
    Review
  14. Article
  15. Article
  16. DNAJ Proteins in neurodegeneration: essential and protective factors.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
    Review
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 4 institutions in 1 country.

José Luis RozasUniversidad de Sevilla and Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas-CIBERNED, 41013 Sevilla, Spain. jrozas@us.es
Leonardo Gómez-Sánchez
Josif Mircheski
Pedro Linares-Clemente
José Luis Nieto-González
M Eugenio Vázquez
Rafael Luján
Rafael Fernández-Chacón
Unidades Centrales Científico-Técnicas · ESConsejo Superior de Investigaciones Científicas · ESUniversidade de Santiago de Compostela · ESUniversity of Castilla-La Mancha · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cysteine string protein-α (CSP-α) is a synaptic vesicle protein that prevents activity-dependent neurodegeneration by poorly understood mechanisms. We have studied the synaptic vesicle cycle at the motor nerve terminals of CSP-α knock-out mice expressing the synaptopHluorin transgene. Mutant nerve terminals fail to sustain prolonged release and the number of vesicles available to be released decreases. Strikingly, the SNARE protein SNAP-25 is dramatically reduced. In addition, endocytosis during the stimulus fails to maintain the size of the recycling synaptic vesicle pool during prolonged stimulation. Upon depolarization, the styryl dye FM 2-10 becomes trapped and poorly releasable. Consistently with the functional results, electron microscopy analysis revealed characteristic features of impaired synaptic vesicle recycling. The unexpected defect in vesicle recycling in CSP-α knock-out mice provides insights into understanding molecular mechanisms of degeneration in motor nerve terminals.

Indexed as

AnimalsExocytosisGreen Fluorescent ProteinsHSP40 Heat-Shock ProteinsMembrane ProteinsMiceMice, KnockoutMice, TransgenicMotor NeuronsMuscle, SkeletalNeuromuscular JunctionRecombinant Fusion ProteinsSynaptic TransmissionSynaptic VesiclesSynaptosomal-Associated Protein 25cysteine string proteinGreen Fluorescent ProteinsHSP40 Heat-Shock ProteinsMembrane ProteinsRecombinant Fusion ProteinssynaptopHIuorinSynaptosomal-Associated Protein 25

Identifiers

PMID22500637
OpenAlexW2074532659

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.