Evidence map›Paper›PMID 37277178›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2023

Dual Regulation of Spine-Specific and Synapse-to-Nucleus Signaling by PKCδ during Plasticity.

Lesley A Colgan, Paula Parra-Bueno, Heather L Holman, Xun Tu, Anant Jain, Mariah F Calubag, Jaime A Misler, Chancellor Gary, Goksu Oz, Irena Suponitsky-Kroyter and 2 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

10 citing papers in PubMed, 15 citations in OpenAlex.

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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

12 authors at 1 institution in 1 country.

Lesley A ColganNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458 Lesley.Colgan@mpfi.org Ryohei.Yasuda@mpfi.org.
Paula Parra-BuenoNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Heather L HolmanNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Xun TuNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Anant JainNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Mariah F CalubagNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Jaime A MislerNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Chancellor GaryNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Goksu OzNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.ORCID 0000-0003-0586-7570
Irena Suponitsky-KroyterNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Elwy OkazNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458.
Ryohei YasudaNeuronal Signal Transduction, Max Planck Florida Institute for Neuroscience, Jupiter, Florida 33458 Lesley.Colgan@mpfi.org Ryohei.Yasuda@mpfi.org.ORCID 0000-0001-6263-9297
Max Planck Florida Institute for Neuroscience · US

Funding

Neuronal Intracellular Signaling Underlying Synaptic, Circuit and Behavioral PlasticityR35NS116804 · NINDS · MAX PLANCK FLORIDA CORPORATION · PI Ryohei Yasuda · 2020 to 2026
$7.8M
Mechanisms of Ras Signaling in Single SynapsesR01MH080047 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2007 to 2023
$6.8M
Spatiotemporal Dynamics of Isozyme-Specific PKC Activity during PlasticityF32MH101954 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI COLGAN, LESLEY A · 2013 to 2014
$115k
NIMH NIH HHS F32 MH101954NIMH NIH HHS R01 MH080047NINDS NIH HHS R35 NS116804
6 · The paper itself

Abstract

The activity-dependent plasticity of synapses is believed to be the cellular basis of learning. These synaptic changes are mediated through the coordination of local biochemical reactions in synapses and changes in gene transcription in the nucleus to modulate neuronal circuits and behavior. The protein kinase C (PKC) family of isozymes has long been established as critical for synaptic plasticity. However, because of a lack of suitable isozyme-specific tools, the role of the novel subfamily of PKC isozymes is largely unknown. Here, through the development of fluorescence lifetime imaging-fluorescence resonance energy transfer activity sensors, we investigate novel PKC isozymes in synaptic plasticity in CA1 pyramidal neurons of mice of either sex. We find that PKCδ is activated downstream of TrkB and DAG production, and that the spatiotemporal nature of its activation depends on the plasticity stimulation. In response to single-spine plasticity, PKCδ is activated primarily in the stimulated spine and is required for local expression of plasticity. However, in response to multispine stimulation, a long-lasting and spreading activation of PKCδ scales with the number of spines stimulated and, by regulating cAMP response-element binding protein activity, couples spine plasticity to transcription in the nucleus. Thus, PKCδ plays a dual functional role in facilitating synaptic plasticity.

Indexed as

IsoenzymesSignal TransductionAnimalsMiceNeuronal PlasticityProtein Kinase CSynapsesIsoenzymesProtein Kinase CCREBFRETPKCplasticitysensorsynapse

Identifiers

PMID37277178
PMCPMC10376934
OpenAlexW4379378018

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.