Evidence map›Paper›PMID 20237283›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Calmodulin controls synaptic strength via presynaptic activation of calmodulin kinase II.

Zhiping P Pang, Peng Cao, Wei Xu, Thomas C Südhof

Abstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing 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

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

63 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. The Role of Calmodulin vs. Synaptotagmin in Exocytosis.Frontiers in molecular neuroscience · 2021
    Review
  9. Article
  10. Elimination ofRNA (New York, N.Y.) · 2020
    Article
  11. Synaptotagmin 1 oligomers clamp and regulate different modes of neurotransmitter release.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Review
  13. CAMK2-Dependent Signaling in Neurons Is Essential for Survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  14. Calcium Sensors in Neuronal Function and Dysfunction.Cold Spring Harbor perspectives in biology · 2019
    Review
  15. Article
  16. PTPσ Drives Excitatory Presynaptic Assembly via Various Extracellular and Intracellular Mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  17. Article
  18. CaThe EMBO journal · 2018
    Article
  19. Article
  20. Analog Signaling With the "Digital" Molecular Switch CaMKII.Frontiers in computational neuroscience · 2018
    Article

3 more citing papers are in PubMed but not listed here.

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.

Zhiping P PangDepartment of Molecular and Cellular Physiology, Stanford University, Palo Alto, California 94304-5543, USA.
Peng Cao
Wei Xu
Thomas C Südhof

Funding

EPILEPSY TRAINING PROGRAMT32NS007280 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1985 to 2020
$3.6M
NINDS NIH HHS 5T32NS007280NINDS NIH HHS T32 NS007280
6 · The paper itself

Abstract

Calmodulin regulates multifarious cellular processes via a panoply of target interactions. However, the central role, multiple isoforms, and complex target interactions of calmodulin make it difficult to examine its precise functions. Here, we analyzed calmodulin function in neurons using lentivirally delivered short-hairpin RNAs that suppressed expression of all calmodulin isoforms by approximately 70%. Calmodulin knockdown did not significantly alter neuronal survival or synapse formation but depressed spontaneous neuronal network activity. Strikingly, calmodulin knockdown decreased the presynaptic release probability almost twofold, without altering the presynaptic readily-releasable vesicle pool or postsynaptic neurotransmitter reception. In calmodulin knockdown neurons, presynaptic release was restored to wild-type levels by expression of constitutively active calmodulin-dependent kinase-IIalpha (CaMKIIalpha); in contrast, in control neurons, expression of constitutively active CaMKIIalpha had no effect on presynaptic release. Viewed together, these data suggest that calmodulin performs a major function in boosting synaptic strength via direct activation of presynaptic calmodulin-dependent kinase II.

Indexed as

AnimalsCalcium-Calmodulin-Dependent Protein Kinase Type 2CalmodulinCell LineCells, CulturedEnzyme ActivationGene Knockdown TechniquesHumansMicePresynaptic TerminalsRNA InterferenceSynapsesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calmodulin

Identifiers

PMID20237283
PMCPMC6632274

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.