Evidence map›Paper›PMID 20140217›Full record

ArticlePloS one2010

Lack of nAChR activity depresses cochlear maturation and up-regulates GABA system components: temporal profiling of gene expression in alpha9 null mice.

Sevin Turcan, Donna K Slonim, Douglas E Vetter

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. 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
0.9field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 18 citations in OpenAlex.

  1. Purinergic Signaling Controls Spontaneous Activity in the Auditory System throughout Early Development.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  2. Article
  3. Frontiers in neuroscience · 2021
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Modulation of hair cell efferents.Hearing research · 2011
    Review
  10. Article
  11. Article
  12. Mining functionally relevant gene sets for analyzing physiologically novel clinical expression data.Pacific Symposium on Biocomputing. Pacific Symposium on Biocomputing · 2011
    Article
  13. Cochlear efferent innervation and function.Current opinion in otolaryngology & head and neck surgery · 2010
    Review
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 1 institution in 1 country.

Sevin TurcanDepartment of Biomedical Engineering, Tufts University, Medford, Massachusetts, United States of America.
Donna K Slonim
Douglas E Vetter
Tufts University · US

Funding

TUSM/T-NEMC CENTER FOR NEUROSCIENCE RESEARCH - Imaging CoreP30NS047243 · NINDS · TUFTS UNIVERSITY BOSTON · PI JACKSON, F ROB · 2003 to 2017
$10.0M
Investigations into the mouse olivocochlear systemR01DC006258 · NIDCD · TUFTS UNIVERSITY BOSTON · PI VETTER, DOUGLAS E · 2004 to 2008
$1.9M
Translational Bioinformatics for Human Developmental GenomicsR01HD058880 · NICHD · TUFTS UNIVERSITY MEDFORD · PI SLONIM, DONNA K. · 2009 to 2012
$1.3M
NICHD NIH HHS R01 HD058880NICHD NIH HHS R01HD058880NIDCD NIH HHS R01 DC006258NIDCD NIH HHS R01DC006258NINDS NIH HHS P30 NS047243NINDS NIH HHS P30NS047243
6 · The paper itself

Abstract

backgroundIt has previously been shown that deletion of chrna9, the gene encoding the alpha9 nicotinic acetylcholine receptor (nAChR) subunit, results in abnormal synaptic terminal structure. Additionally, all nAChR-mediated cochlear activity is lost, as characterized by a failure of the descending efferent system to suppress cochlear responses to sound. In an effort to characterize the molecular mechanisms underlying the structural and functional consequences following loss of alpha9 subunit expression, we performed whole-transcriptome gene expression analyses on cochleae of wild type and alpha9 knockout (alpha9(-/-)) mice during postnatal days spanning critical periods of synapse formation and maturation. PRINCIPAL

findingsData revealed that loss of alpha9 receptor subunit expression leads to an up-regulation of genes involved in synaptic transmission and ion channel activity. Unexpectedly, loss of alpha9 receptor subunit expression also resulted in an increased expression of genes encoding GABA receptor subunits and the GABA synthetic enzyme, glutamic acid decarboxylase. These data suggest the existence of a previously unrecognized association between the nicotinic cholinergic and GABAergic systems in the cochlea. Computational analyses have highlighted differential expression of several gene sets upon loss of nicotinic cholinergic activity in the cochlea. Time-series analysis of whole transcriptome patterns, represented as self-organizing maps, revealed a disparate pattern of gene expression between alpha9(-/-) and wild type cochleae at the onset of hearing (P13), with knockout samples resembling immature postnatal ages.

conclusionsWe have taken a systems biology approach to provide insight into molecular programs influenced by the loss of nicotinic receptor-based cholinergic activity in the cochlea and to identify candidate genes that may be involved in nicotinic cholinergic synapse formation, stabilization or function within the inner ear. Additionally, our data indicate a change in the GABAergic system upon loss of alpha9 nicotinic receptor subunit within the cochlea.

Indexed as

Up-RegulationAnimalsBlotting, WesternCluster AnalysisCochleaGene Expression ProfilingGene Expression Regulation, DevelopmentalImmunohistochemistryMiceMice, KnockoutNeuronsOligonucleotide Array Sequence AnalysisProtein SubunitsReceptors, GABAReceptors, NicotinicReverse Transcriptase Polymerase Chain ReactionChrna9 protein, mouseProtein SubunitsReceptors, GABAReceptors, Nicotinic

Identifiers

PMID20140217
PMCPMC2816210
OpenAlexW2049473433

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.