Evidence map›Paper›PMID 21697360›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Differential control of presynaptic CaMKII activation and translocation to active zones.

Dinara Shakiryanova, Takako Morimoto, Chaoming Zhou, Amit K Chouhan, Stephan J Sigrist, Akinao Nose, Gregory T Macleod, David L Deitcher, Edwin S Levitan

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
–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

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

24 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. The Long 3'UTR mRNA ofThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  14. Article
  15. Sexual Dimorphism in a Reciprocal Interaction of Ryanodine and IPThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    Article
  16. Article
  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

9 authors.

Dinara ShakiryanovaDepartment of Pharmacology and Chemical Biology, University of Pittsburgh, Pittsburgh, Pennsylvania 15261, USA.
Takako Morimoto
Chaoming Zhou
Amit K Chouhan
Stephan J Sigrist
Akinao Nose
Gregory T Macleod
David L Deitcher
Edwin S Levitan

Funding

Dense-Core Vesicle Circulation, Capture and Synaptic Neuropeptide ReleaseR01NS032385 · NINDS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI EDWIN S LEVITAN · 1995 to 2026
$13.0M
The multiple roles of mitochondria in synaptic transmissionR01NS061914 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI MACLEOD, GREGORY TALISKER · 2008 to 2016
$2.6M
NINDS NIH HHS R01 NS032385NINDS NIH HHS R01 NS061914NINDS NIH HHS R01 NS32385
6 · The paper itself

Abstract

The release of neurotransmitters, neurotrophins, and neuropeptides is modulated by Ca(2+) mobilization from the endoplasmic reticulum (ER) and activation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). Furthermore, when neuronal cultures are subjected to prolonged depolarization, presynaptic CaMKII redistributes from the cytoplasm to accumulate near active zones (AZs), a process that is reminiscent of CaMKII translocation to the postsynaptic side of the synapse. However, it is not known how presynaptic CaMKII activation and translocation depend on neuronal activity and ER Ca(2+) release. Here these issues are addressed in Drosophila motoneuron terminals by imaging a fluorescent reporter of CaMKII activity and subcellular distribution. We report that neuronal excitation acts with ER Ca(2+) stores to induce CaMKII activation and translocation to a subset of AZs. Surprisingly, activation is slow, reflecting T286 autophosphorylation and the function of presynaptic ER ryanodine receptors (RyRs) and inositol trisphosphate receptors (IP3Rs). Furthermore, translocation is not simply proportional to CaMKII activity, as T286 autophosphorylation promotes activation, but does not affect translocation. In contrast, RNA interference-induced knockdown of the AZ scaffold protein Bruchpilot disrupts CaMKII translocation without affecting activation. Finally, RyRs comparably stimulate both activation and translocation, but IP3Rs preferentially promote translocation. Thus, Ca(2+) provided by different presynaptic ER Ca(2+) release channels is not equivalent. These results suggest that presynaptic CaMKII activation depends on autophosphorylation and global Ca(2+) in the terminal, while translocation to AZs requires Ca(2+) microdomains generated by IP3Rs.

Indexed as

AnimalsCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2Cells, CulturedDrosophilaEnzyme ActivationFeedback, PhysiologicalMotor NeuronsPresynaptic TerminalsProtein TransportSynaptic TransmissionCalciumCalcium-Calmodulin-Dependent Protein Kinase Type 2

Identifiers

PMID21697360
PMCPMC3123710

What OpenQuestion holds

Textmetadata
LicenceTDM
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.