Evidence map›Paper›PMID 25698934›Full record

ArticleFrontiers in cellular neuroscience2015

Bruchpilot and Synaptotagmin collaborate to drive rapid glutamate release and active zone differentiation.

Mila M Paul, Martin Pauli, Nadine Ehmann, Stefan Hallermann, Markus Sauer, Robert J Kittel, Manfred Heckmann

Abstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
–field-weighted citation impact
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

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3 · Its place in the literature

Who cites it

27 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Neto proteins differentially modulate the gating properties ofbioRxiv : the preprint server for biology · 2024
    Article
  7. Article
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  9. Article
  10. Single-Molecule Localization Microscopy of Presynaptic Active Zones inInternational journal of molecular sciences · 2023
    Article
  11. Article
  12. Glutamatergic Synapse Dysfunction inFrontiers in molecular neuroscience · 2022
    Article
  13. Separation of presynaptic CaProceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  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

7 authors.

Mila M PaulDepartment of Neurophysiology, Institute of Physiology, Julius-Maximilians-University Würzburg Würzburg, Germany.
Martin PauliDepartment of Neurophysiology, Institute of Physiology, Julius-Maximilians-University Würzburg Würzburg, Germany.
Nadine EhmannDepartment of Neurophysiology, Institute of Physiology, Julius-Maximilians-University Würzburg Würzburg, Germany.
Stefan HallermannCarl-Ludwig-Institute for Physiology, University of Leipzig Leipzig, Germany.
Markus SauerDepartment of Biotechnology and Biophysics, Julius-Maximilians-University Würzburg Würzburg, Germany.
Robert J KittelDepartment of Neurophysiology, Institute of Physiology, Julius-Maximilians-University Würzburg Würzburg, Germany.
Manfred HeckmannDepartment of Neurophysiology, Institute of Physiology, Julius-Maximilians-University Würzburg Würzburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The active zone (AZ) protein Bruchpilot (Brp) is essential for rapid glutamate release at Drosophila melanogaster neuromuscular junctions (NMJs). Quantal time course and measurements of action potential-waveform suggest that presynaptic fusion mechanisms are altered in brp null mutants (brp(69) ). This could account for their increased evoked excitatory postsynaptic current (EPSC) delay and rise time (by about 1 ms). To test the mechanism of release protraction at brp(69) AZs, we performed knock-down of Synaptotagmin-1 (Syt) via RNAi (syt(KD) ) in wildtype (wt), brp(69) and rab3 null mutants (rab3(rup) ), where Brp is concentrated at a small number of AZs. At wt and rab3(rup) synapses, syt(KD) lowered EPSC amplitude while increasing rise time and delay, consistent with the role of Syt as a release sensor. In contrast, syt(KD) did not alter EPSC amplitude at brp(69) synapses, but shortened delay and rise time. In fact, following syt(KD) , these kinetic properties were strikingly similar in wt and brp(69) , which supports the notion that Syt protracts release at brp(69) synapses. To gain insight into this surprising role of Syt at brp(69) AZs, we analyzed the structural and functional differentiation of synaptic boutons at the NMJ. At 'tonic' type Ib motor neurons, distal boutons contain more AZs, more Brp proteins per AZ and show elevated and accelerated glutamate release compared to proximal boutons. The functional differentiation between proximal and distal boutons is Brp-dependent and reduced after syt(KD) . Notably, syt(KD) boutons are smaller, contain fewer Brp positive AZs and these are of similar number in proximal and distal boutons. In addition, super-resolution imaging via dSTORM revealed that syt(KD) increases the number and alters the spatial distribution of Brp molecules at AZs, while the gradient of Brp proteins per AZ is diminished. In summary, these data demonstrate that normal structural and functional differentiation of Drosophila AZs requires concerted action of Brp and Syt.

Indexed as

active zoneBruchpilotdSTORMneurotransmitter releasepresynaptic differentiationsynaptic delaysynaptotagmin

Identifiers

PMID25698934
PMCPMC4318344

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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.