Evidence map›Paper›PMID 33397944›Full record

ArticleNature communications2021

Sensory input drives rapid homeostatic scaling of the axon initial segment in mouse barrel cortex.

Nora Jamann, Dominik Dannehl, Nadja Lehmann, Robin Wagener, Corinna Thielemann, Christian Schultz, Jochen Staiger, Maarten H P Kole, Maren Engelhardt

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed
9.4field-weighted citation impact, top 1% 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

65 citing papers in PubMed, 106 citations in OpenAlex.

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  12. Hippocampal Chandelier Cells Modulate Seizure Susceptibility and Severity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  13. Article
  14. Impaired AIS plasticity in ankyrin-G mutant mice alters cortical excitability and behavior.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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5 more citing papers are in PubMed but not listed here.

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

9 authors at 4 institutions in 2 countries.

Nora JamannAxonal Signaling Group, Netherlands Institute for Neurosciences (NIN), Royal Netherlands Academy for Arts and Sciences (KNAW), Amsterdam, The Netherlands.ORCID 0000-0002-8875-4522
Dominik DannehlInstitute of Neuroanatomy, Mannheim Center for Translational Neuroscience (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Nadja LehmannInstitute of Neuroanatomy, Mannheim Center for Translational Neuroscience (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.ORCID 0000-0003-4801-3057
Robin WagenerClinic of Neurology, University Hospital Heidelberg, Heidelberg, Germany.
Corinna ThielemannInstitute of Neuroanatomy, Mannheim Center for Translational Neuroscience (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Christian SchultzInstitute of Neuroanatomy, Mannheim Center for Translational Neuroscience (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Jochen StaigerInstitute of Neuroanatomy, University Medical Center, Georg August University of Göttingen, Göttingen, Germany.
Maarten H P KoleAxonal Signaling Group, Netherlands Institute for Neurosciences (NIN), Royal Netherlands Academy for Arts and Sciences (KNAW), Amsterdam, The Netherlands. m.kole@nin.knaw.nl.ORCID 0000-0002-3883-5682
Maren EngelhardtInstitute of Neuroanatomy, Mannheim Center for Translational Neuroscience (MCTN), Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany. maren.engelhardt@medma.uni-heidelberg.de.
Heidelberg University · DENetherlands Institute for Neuroscience · NLUniversity of Göttingen · DEUniversity of Mannheim · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The axon initial segment (AIS) is a critical microdomain for action potential initiation and implicated in the regulation of neuronal excitability during activity-dependent plasticity. While structural AIS plasticity has been suggested to fine-tune neuronal activity when network states change, whether it acts in vivo as a homeostatic regulatory mechanism in behaviorally relevant contexts remains poorly understood. Using the mouse whisker-to-barrel pathway as a model system in combination with immunofluorescence, confocal analysis and electrophysiological recordings, we observed bidirectional AIS plasticity in cortical pyramidal neurons. Furthermore, we find that structural and functional AIS remodeling occurs in distinct temporal domains: Long-term sensory deprivation elicits an AIS length increase, accompanied with an increase in neuronal excitability, while sensory enrichment results in a rapid AIS shortening, accompanied by a decrease in action potential generation. Our findings highlight a central role of the AIS in the homeostatic regulation of neuronal input-output relations.

Indexed as

HomeostasisAgingAnimalsAxon Initial SegmentCerebral CortexExploratory BehaviorMiceMice, Inbred C57BLNeuronal PlasticityPyramidal CellsSensory DeprivationTime FactorsVibrissae

Identifiers

PMID33397944
PMCPMC7782484
OpenAlexW3118723661

What OpenQuestion holds

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LicenceCC BY
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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.