Evidence map›Paper›PMID 12040073›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002

bcl-2 Overexpression eliminates deprivation-induced cell death of brainstem auditory neurons.

Sam P Mostafapour, N Mae Del Puerto, Edwin W Rubel

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.3field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 65 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Neuronal Cell Death.Physiological reviews · 2018
    Review
  5. Article
  6. Selective deletion of cochlear hair cells causes rapid age-dependent changes in spiral ganglion and cochlear nucleus neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  7. Article
  8. Review
  9. Heterogeneous calretinin expression in the avian cochlear nucleus angularis.Journal of the Association for Research in Otolaryngology : JARO · 2014
    Article
  10. Transient, afferent input-dependent, postnatal niche for neural progenitor cells in the cochlear nucleus.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  11. Mature neurons: equipped for survival.Cell death & disease · 2013
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Article
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.

Sam P MostafapourVirginia Merrill Bloedel Hearing Research Center and Department of Otolaryngology, Head and Neck Surgery, University of Washington, Seattle, Washington 98195.
N Mae Del Puerto
Edwin W Rubel
University of Washington · US

Funding

Motley Diversity SupplementR01DC003829 · NIDCD · UNIVERSITY OF WASHINGTON · PI RUBEL, EDWIN W · 1999 to 2014
$6.0M
NIDCD NIH HHS DC03829NIDCD NIH HHS R01 DC003829
6 · The paper itself

Abstract

Deprivation of afferent input in young animals results in transneuronal degeneration of postsynaptic sensory neurons in a variety of species and sensory pathways. Transneuronal degeneration is generally not seen in adult animals. The cellular and molecular basis for this dramatic developmental change in susceptibility is not understood. One possibility is that genes involved in the apoptotic process are involved in determining cell death or survival after afferent deprivation. To further investigate this possibility, we performed unilateral cochlear ablation on wild-type and bcl-2-overexpressing mice at a variety of ages. In postnatal day 5 (P5) or P8 wild-type mice, cochlea removal resulted in a 54% or 31% neuronal loss in the anteroventral cochlear nucleus (AVCN), respectively. When the same manipulation is performed on a P30 mouse, no loss of AVCN neurons occurs. This confirmed a rather abrupt change in the sensitivity to disruption of afferent input, a critical period. However, in littermates expressing bcl-2 under a neuron-specific enolase promoter, no significant loss of AVCN neurons was observed at any age after unilateral cochlear ablation. Furthermore, wild-type mice demonstrate rapid expression of activated caspase-3 in AVCN neurons within hours of deafferentation, whereas bcl-2-overexpressing mice do not. This suggests that bcl-2 can influence cell survival after removal of afferent input during the critical period and is consistent with the hypothesis that caspase-3 is one effector of cell death under these circumstances. These data are the first to indicate that known apoptotic mediators can play a role in central neuronal plasticity in models of afferent deprivation.

Indexed as

Age FactorsAnimalsApoptosisAuditory PathwaysBrain StemCaspase 3CaspasesCell CountCell SurvivalCochlear NucleusCritical Period, PsychologicalDeafnessGene ExpressionHumansMiceMice, TransgenicCASP3 protein, humanCasp3 protein, mouseCaspase 3CaspasesProto-Oncogene Proteins c-bcl-2

Identifiers

PMID12040073
PMCPMC6758828
OpenAlexW2164443122

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.