Evidence map›Paper›PMID 25164660›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014

Synaptopodin regulates spine plasticity: mediation by calcium stores.

Eduard Korkotian, Michael Frotscher, Menahem Segal

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

58 citing papers in PubMed, 95 citations in OpenAlex.

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  12. Synaptopodin: a key regulator of Hebbian plasticity.Frontiers in cellular neuroscience · 2024
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  17. Stabilization of Spine Synaptopodin by mGluR1 Is Required for mGluR-LTD.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
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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

3 authors at 2 institutions in 2 countries.

Eduard KorkotianDepartment of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel, and.
Michael FrotscherInstitute for Structural Neurobiology, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, 20251 Hamburg, Germany.
Menahem SegalDepartment of Neurobiology, The Weizmann Institute, Rehovot 76100, Israel, and Menahem.segal@weizmann.ac.il.
Weizmann Institute of Science · ILUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of synaptopodin (SP), an actin-binding protein residing in dendritic spines, in synaptic plasticity was studied in dissociated cultures of hippocampus taken from control and SP knock-out (SPKO) mice. Unlike controls, SPKO cultures were unable to express changes in network activity or morphological plasticity after intense activation of their NMDA receptors. SPKO neurons were transfected with SP-GFP, such that the only SP resident in these neurons is the fluorescent species. The localization and intensity of the transfected SP were similar to that of the native one. Because less than half of the spines in the transfected neurons contained SP, comparisons were made between SP-containing (SP(+)) and SP lacking (SP(-)) spines in the same dendritic segments. Synaptic plasticity was induced either in the entire network by facilitation of the activation of the NMDA receptor, or specifically by local flash photolysis of caged glutamate. After activation, spines that were endowed with SP puncta were much more likely to expand than SP(-) spines. The spine expansion was suppressed by thapsigargin, which disables calcium stores. The mechanism through which SP may promote plasticity is indicated by the observations that STIM-1, the sensor of calcium concentration in stores, and Orai-1, the calcium-induced calcium entry channel, are colocalized with SP, in the same dendritic spines. The structural basis of SP is likely to be the spine apparatus, found in control but not in SPKO cells. These results indicate that SP has an essential, calcium store-related role in regulating synaptic plasticity in cultured hippocampal neurons.

Indexed as

AnimalsCalciumDendritic SpinesHippocampusImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutMicrofilament ProteinsMicroscopy, ConfocalNeuronal PlasticityPatch-Clamp TechniquesSynapsesTransfectionCalciumMicrofilament ProteinsSynpo protein, mousecalcium storesdendritic spinemorphological plasticityOrai1STIM1synaptopodin

Identifiers

PMID25164660
PMCPMC6608418
OpenAlexW1984924474

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.