Evidence map›Paper›PMID 26916562›Full record

ArticleActa neuropathologica communications2016

A general homeostatic principle following lesion induced dendritic remodeling.

Steffen Platschek, Hermann Cuntz, Mario Vuksic, Thomas Deller, Peter Jedlicka

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing 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

13 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.

Steffen PlatschekInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt, D-60590, Frankfurt/Main, Germany.
Hermann CuntzInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt, D-60590, Frankfurt/Main, Germany. hermann.neuro@gmail.com.
Mario VuksicInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt, D-60590, Frankfurt/Main, Germany.
Thomas DellerInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt, D-60590, Frankfurt/Main, Germany.
Peter JedlickaInstitute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University Frankfurt, D-60590, Frankfurt/Main, Germany. jedlicka@em.uni-frankfurt.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionNeuronal death and subsequent denervation of target areas are hallmarks of many neurological disorders. Denervated neurons lose part of their dendritic tree, and are considered "atrophic", i.e. pathologically altered and damaged. The functional consequences of this phenomenon are poorly understood.

resultsUsing computational modelling of 3D-reconstructed granule cells we show that denervation-induced dendritic atrophy also subserves homeostatic functions: By shortening their dendritic tree, granule cells compensate for the loss of inputs by a precise adjustment of excitability. As a consequence, surviving afferents are able to activate the cells, thereby allowing information to flow again through the denervated area. In addition, action potentials backpropagating from the soma to the synapses are enhanced specifically in reorganized portions of the dendritic arbor, resulting in their increased synaptic plasticity. These two observations generalize to any given dendritic tree undergoing structural changes.

conclusionsStructural homeostatic plasticity, i.e. homeostatic dendritic remodeling, is operating in long-term denervated neurons to achieve functional homeostasis.

Indexed as

Action PotentialsAnimalsBiophysicsBrain InjuriesComputer SimulationDendritesDenervationElectric StimulationGreen Fluorescent ProteinsHomeostasisMiceMice, TransgenicModels, NeurologicalNeuronsStatistics, NonparametricSynapsesGreen Fluorescent Proteins

Identifiers

PMID26916562
PMCPMC4766619

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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.