Evidence map›Paper›PMID 10811820›Full record

ArticleThe Journal of cell biology2000

Intracellular Ca(2+) and Ca(2+)/calmodulin-dependent kinase II mediate acute potentiation of neurotransmitter release by neurotrophin-3.

X He, F Yang, Z Xie, B Lu

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of cell biology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

26 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. TRPC5 channel is the mediator of neurotrophin-3 in regulating dendritic growth via CaMKIIα in rat hippocampal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  7. Article
  8. Differential control of presynaptic CaMKII activation and translocation to active zones.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    Article
  9. Calcium/calmodulin kinase II-dependent acetylcholine receptor cycling at the mammalian neuromuscular junction in vivo.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010
    Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Article
  15. Presynaptic ryanodine receptor-activated calmodulin kinase II increases vesicle mobility and potentiates neuropeptide release.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  16. Schwann cell-derived factors modulate synaptic activities at developing neuromuscular synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007
    Article
  17. Review
  18. Article
  19. Pathophysiological mechanisms for actions of the neurotrophins.Brain pathology (Zurich, Switzerland) · 2006
    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

4 authors at 2 institutions in 1 country.

X HeUnit on Synapse Development and Plasticity, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 20892, USA.
F Yang
Z Xie
B Lu
Eunice Kennedy Shriver National Institute of Child Health and Human Development · USNational Institutes of Health · US

Funding

Molecular Mechanisms Of Synapse Development &PlasticityZ01HD000714 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI LU, BAI · 1996 to 2008
$2.7M
6 · The paper itself

Abstract

Neurotrophins have been shown to acutely modulate synaptic transmission in a variety of systems, but the underlying signaling mechanisms remain unclear. Here we provide evidence for an unusual mechanism that mediates synaptic potentiation at the neuromuscular junction (NMJ) induced by neurotrophin-3 (NT3), using Xenopus nerve-muscle co-culture. Unlike brain-derived neurotrophic factor (BDNF), which requires Ca(2+) influx for its acute effect, NT3 rapidly enhances spontaneous transmitter release at the developing NMJ even when Ca(2+) influx is completely blocked, suggesting that the NT3 effect is independent of extracellular Ca(2+). Depletion of intracellular Ca(2+) stores, or blockade of inositol 1, 4, 5-trisphosphate (IP3) or ryanodine receptors, prevents the NT3-induced synaptic potentiation. Blockade of IP3 receptors can not prevent BDNF-induced potentiation, suggesting that BDNF and NT3 use different mechanisms to potentiate transmitter release. Inhibition of Ca(2+)/calmodulin-dependent kinase II (CaMKII) completely blocks the acute effect of NT3. Furthermore, the NT3-induced potentiation requires a continuous activation of CaMKII, because application of the CaMKII inhibitor KN62 reverses the previously established NT3 effect. Thus, NT3 potentiates neurotransmitter secretion by stimulating Ca(2+) release from intracellular stores through IP3 and/or ryanodine receptors, leading to an activation of CaMKII.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channel BlockersCalcium ChannelsCarrier ProteinsCells, CulturedCoculture TechniquesElectric ConductivityEnzyme ActivationInositol 1,4,5-Trisphosphate ReceptorsIntracellular Signaling Peptides and ProteinsNeuromuscular JunctionNeurotransmitter AgentsBrain-Derived Neurotrophic FactorCalciumCalcium-Calmodulin-Dependent Protein KinasesCalcium-Calmodulin-Dependent Protein Kinase Type 2Calcium Channel BlockersCalcium ChannelsCAMK2N2 protein, humanCarrier ProteinsInositol 1,4,5-Trisphosphate ReceptorsIntracellular Signaling Peptides and ProteinsITPR1 protein, humanNeurotransmitter AgentsNeurotrophin 3Receptors, Cytoplasmic and NuclearRyanodine Receptor Calcium Release Channel

Identifiers

PMID10811820
PMCPMC2174561
OpenAlexW2001385914

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.