Evidence map›Paper›PMID 33789115›Full record

ArticleCell reports2021

EphrinB2 and GRIP1 stabilize mushroom spines during denervation-induced homeostatic plasticity.

Diane Bissen, Maximilian Ken Kracht, Franziska Foss, Jan Hofmann, Amparo Acker-Palmer

Abstract read
In one paragraph

Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing 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

8 citing papers in PubMed.

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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

5 authors.

Diane BissenInstitute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany; Max Planck Institute for Brain Research, Max von Laue Str. 4, 60438 Frankfurt am Main, Germany.
Maximilian Ken KrachtInstitute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany.
Franziska FossInstitute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany.
Jan HofmannInstitute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany.
Amparo Acker-PalmerInstitute of Cell Biology and Neuroscience and Buchmann Institute for Molecular Life Sciences (BMLS), University of Frankfurt, Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany; Max Planck Institute for Brain Research, Max von Laue Str. 4, 60438 Frankfurt am Main, Germany; Cardio-Pulmonary Institute (CPI), Max-von-Laue-Str. 15, 60438 Frankfurt am Main, Germany. Electronic address: acker-palmer@bio.uni-frankfurt.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Despite decades of work, much remains elusive about molecular events at the interplay between physiological and structural changes underlying neuronal plasticity. Here, we combined repetitive live imaging and expansion microscopy in organotypic brain slice cultures to quantitatively characterize the dynamic changes of the intracellular versus surface pools of GluA2-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) across the different dendritic spine types and the shaft during hippocampal homeostatic plasticity. Mechanistically, we identify ephrinB2 and glutamate receptor interacting protein (GRIP) 1 as mediating AMPAR relocation to the mushroom spine surface following lesion-induced denervation. Moreover, stimulation with the ephrinB2 specific receptor EphB4 not only prevents the lesion-induced disappearance of mushroom spines but is also sufficient to shift AMPARs to the surface and rescue spine recovery in a GRIP1 dominant-negative background. Thus, our results unravel a crucial role for ephrinB2 during homeostatic plasticity and identify a potential pharmacological target to improve dendritic spine plasticity upon injury.

Indexed as

HomeostasisAdaptor Proteins, Signal TransducingAnimalsCell MembraneDendritic SpinesDenervationEphrin-B2MiceMice, Inbred C57BLNerve Tissue ProteinsNeuronal PlasticityReceptor, EphB4Receptors, AMPAAdaptor Proteins, Signal TransducingEphb4 protein, mouseEphrin-B2Grip1 protein, mouseNerve Tissue ProteinsReceptor, EphB4Receptors, AMPAAMPA receptorsdenervationEphB4ephrinB2expansion microscopyGRIP1hippocampushomeostatic plasticitymushroom spinesorganotypic slice cultures

Identifiers

PMID33789115
PMCPMC8028307

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Registered trials

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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.