Evidence map›Paper›PMID 21658591›Full record

ArticleNeuron2011

Calcium-dependent isoforms of protein kinase C mediate posttetanic potentiation at the calyx of Held.

Diasynou Fioravante, YunXiang Chu, Michael H Myoga, Michael Leitges, Wade G Regehr

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

39 citing papers in PubMed, 53 citations in OpenAlex.

  1. Munc13-1 couples DAG and CaScience advances · 2026
    Article
  2. CaCell reports · 2025
    Article
  3. Article
  4. Article
  5. Sex- and subtype-specific adaptations in excitatory signaling onto deep-layer prelimbic cortical pyramidal neurons after chronic alcohol exposure.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  6. Presynaptic Short-Term Plasticity Persists in the Absence of PKC Phosphorylation of Munc18-1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Single Bursts of Individual Granule Cells Functionally Rearrange Feedforward Inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Dissecting the Role of P/Q-Type Calcium Channels in Corticothalamic Circuit Dysfunction and Absence Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Review
  19. Phosphorylation of synaptotagmin-1 controls a post-priming step in PKC-dependent presynaptic plasticity.Proceedings of the National Academy of Sciences of the United States of America · 2016
    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

5 authors at 2 institutions in 2 countries.

Diasynou FioravanteDepartment of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.
YunXiang Chu
Michael H Myoga
Michael Leitges
Wade G Regehr
Harvard University · USUniversity of Oslo · NO

Funding

PHD TRAINING IN NEUROSCIENCET32MH020017 · NIMH · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI JOHN ASSAD · 1997 to 2026
$15.8M
Short-Term Synaptic Plasticity in the CNSR01NS032405 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI REGEHR, WADE G · 1995 to 2016
$4.8M
Short-Term Synaptic Plasticity in the CNSR37NS032405 · NINDS · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI REGEHR, WADE G · 2005 to 2011
$4.7M
NIMH NIH HHS T32 MH020017NINDS NIH HHS R01 NS032405NINDS NIH HHS R37 NS032405
6 · The paper itself

Abstract

High-frequency stimulation leads to a transient increase in the amplitude of evoked synaptic transmission that is known as posttetanic potentiation (PTP). Here we examine the roles of the calcium-dependent protein kinase C isoforms PKCα and PKCβ in PTP at the calyx of Held synapse. In PKCα/β double knockouts, 80% of PTP is eliminated, whereas basal synaptic properties are unaffected. PKCα and PKCβ produce PTP by increasing the size of the readily releasable pool of vesicles evoked by high-frequency stimulation and by increasing the fraction of this pool released by the first stimulus. PKCα and PKCβ do not facilitate presynaptic calcium currents. The small PTP remaining in double knockouts is mediated partly by an increase in miniature excitatory postsynaptic current amplitude and partly by a mechanism involving myosin light chain kinase. These experiments establish that PKCα and PKCβ are crucial for PTP and suggest that long-lasting presynaptic calcium increases produced by tetanic stimulation may activate these isoforms to produce PTP.

Indexed as

AnimalsAzepinesBiophysicsCalciumElectric StimulationExcitatory Postsynaptic PotentialsIn Vitro TechniquesMiceMice, Inbred C57BLMice, KnockoutPatch-Clamp TechniquesPhorbol EstersPresynaptic TerminalsProtein Kinase CProtein Kinase C-alphaProtein Kinase C betaAzepinesCalciumML 9Phorbol EstersProtein Kinase CProtein Kinase C-alphaProtein Kinase C betaSlc17a7 protein, mouseTeprotideVesicular Glutamate Transport Protein 1

Identifiers

PMID21658591
PMCPMC3113702
OpenAlexW2068105241

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.