Evidence map›Paper›PMID 21632949›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Cav1.3 calcium channels are required for normal development of the auditory brainstem.

Jan J Hirtz, Michael Boesen, Nadine Braun, Joachim W Deitmer, Florian Kramer, Christian Lohr, Britta Müller, Hans Gerd Nothwang, Jörg Striessnig, Stefan Löhrke and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
4.6field-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

57 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Deletion of the Voltage-Gated Calcium Channel Gene, CaCerebellum (London, England) · 2025
    Article
  3. Strengthening Medial Olivocochlear Feedback Reduces the Developmental Impact of Early Noise Exposure.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
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  16. Auditory brainstem development of naked mole-rats (Proceedings. Biological sciences · 2022
    Article
  17. Loss of miR-183/96 Alters Synaptic Strength via Presynaptic and Postsynaptic Mechanisms at a Central Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
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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

11 authors at 3 institutions in 2 countries.

Jan J HirtzDepartment of Biology, University of Kaiserslautern, D-67653 Kaiserslautern, Germany.
Michael Boesen
Nadine Braun
Joachim W Deitmer
Florian Kramer
Christian Lohr
Britta Müller
Hans Gerd Nothwang
Jörg Striessnig
Stefan Löhrke
Eckhard Friauf
University of Kaiserslautern · DECarl von Ossietzky Universität Oldenburg · DEUniversität Innsbruck · AT

Funding

Austrian Science Fund FWF P 20670
6 · The paper itself

Abstract

Within the Ca(v)1 family of voltage-gated calcium channels, Ca(v)1.2 and Ca(v)1.3 channels are the predominant subtypes in the brain. Whereas specific functions for each subtype were described in the adult brain, their role in brain development is poorly understood. Here we assess the role of Ca(v)1.3 subunits in the activity-dependent development of the auditory brainstem. We used Ca(v)1.3-deficient (Ca(v)1.3(-/-)) mice because these mice lack cochlea-driven activity that deprives the auditory centers from peripheral input. We found a drastically reduced volume in all auditory brainstem centers (range 25-59%, total 35%), which was manifest before hearing onset. A reduction was not obvious outside the auditory system. The lateral superior olive (LSO) was strikingly malformed in Ca(v)1.3(-/-) mice and had fewer neurons (1/3 less). The remaining LSO neurons displayed normal dendritic trees and received functional glutamatergic input, yet they fired action potentials predominantly with a multiple pattern upon depolarization, in contrast to the single firing pattern prevalent in controls. The latter finding appears to be due to a reduction of dendrototoxin-sensitive potassium conductances, presumably mediated through the K(v)1.2 subtype. Fura2 imaging provided evidence for functional Ca(v)1.3 channels in the LSO of wild-type mice. Our results imply that Ca(v)1.3 channels are indispensable for the development of the central auditory system. We propose that the unique LSO phenotype in Ca(v)1.3(-/-) mice, which hitherto was not described in other hereditary deafness models, is caused by the synergistic contribution of two factors: on-site loss of Ca(v)1.3 channels in the neurons plus lack of peripheral input.

Indexed as

Action PotentialsAnimalsAtrophyBrain StemCalcium Channels, L-TypeCell CountElapid VenomsFemaleMaleMiceMice, Inbred C57BLMice, KnockoutNeuronsPatch-Clamp TechniquesReceptors, N-Methyl-D-AspartateCacna1d protein, mouseCalcium Channels, L-TypedendrotoxinElapid VenomsReceptors, N-Methyl-D-Aspartate

Identifiers

PMID21632949
PMCPMC6622878
OpenAlexW2026123114

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.