Evidence map›Paper›PMID 11264301›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001

Multiple distinct signal pathways, including an autocrine neurotrophic mechanism, contribute to the survival-promoting effect of depolarization on spiral ganglion neurons in vitro.

M R Hansen, X M Zha, J Bok, S H Green

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
3.3field-weighted citation impact, top 7% 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

50 citing papers in PubMed, 134 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Dynamic Heterogeneity Shapes Patterns of Spiral Ganglion Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. CaBP1 regulates CaMolecular and cellular neurosciences · 2018
    Article
  11. Article
  12. Photopolymerized Microfeatures Guide Adult Spiral Ganglion and Dorsal Root Ganglion Neurite Growth.Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology · 2018
    Article
  13. Article
  14. Article
  15. Article
  16. AP-1 Transcription Factors Mediate BDNF-Positive Feedback Loop in Cortical Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  17. Article
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  19. 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

4 authors at 1 institution in 1 country.

M R HansenDepartment of Biological Sciences, University of Iowa, Iowa City, Iowa 52242, USA.
X M Zha
J Bok
S H Green
University of Iowa · US

Funding

Research Training Program in OtolaryngologyT32DC000040 · NIDCD · UNIVERSITY OF IOWA · PI HANSEN, MARLAN R · 1993 to 2025
$5.4M
Stimuli promoting the survival of spiral ganglion neuronsR01DC002961 · NIDCD · UNIVERSITY OF IOWA · PI GREEN, STEVEN H · 1996 to 2011
$3.6M
SITE SPECIFIC ANTIINSULIN RECEPTOR ANTIBODIESP30DK025295 · NIDDK · UNIVERSITY OF IOWA · PI BAR, ROBERT S · 1986 to 2002
$2.6M
NIDCD NIH HHS DC00040NIDCD NIH HHS DC02961NIDCD NIH HHS R01 DC002961NIDCD NIH HHS T32 DC000040NIDDK NIH HHS DK25295
6 · The paper itself

Abstract

We have shown previously that BDNF, neurotrophin-3 (NT-3), chlorphenylthio-cAMP (cpt-cAMP) (a permeant cAMP analog), and membrane depolarization promote spiral ganglion neuron (SGN) survival in vitro in an additive manner, depolarization having the greatest efficacy. Expression of both BDNF and of NT-3 is detectable in cultured SGNs after plating in either depolarizing or nondepolarizing medium. These neurotrophins promote survival by an autocrine mechanism; TrkB-IgG or TrkC-IgG, which block neurotrophin binding to, respectively, TrkB and TrkC, partially inhibit the trophic effect of depolarization. The mitogen-activated protein kinase kinase inhibitor PD98059 and the phosphatidylinositol-3-OH kinase inhibitor LY294002 both abolish trophic support by neurotrophins but only partially inhibit support by depolarization. Inhibition by these compounds is not additive with inhibition by Trk-IgGs. The cAMP antagonist Rp-adenosine-3',5'-cyclic-phosphorothioate (Rp-cAMPS) abolishes survival attributable to cpt-cAMP but has no effect on that attributable to neurotrophins, nor do inhibitors of neurotrophin-dependent survival affect survival attributable to cpt-cAMP. However, Rp-cAMPS does partially inhibit depolarization-dependent survival, an inhibition that is additive with that by Trk-IgGs, PD98059, or LY294002. Moreover, Rp-cAMPS prevents depolarization-dependent survival of PC12 cells maintained in subthreshold levels of NGF. Inhibition of Ca(2+)/calmodulin-dependent protein kinases (CaMKs) with KN-62 reduces SGN survival independently of Rp-cAMPS, Trk-IgGs, and LY294002 and additively with them. Combined inhibition of Trk, cAMP, and CaMK signaling prevents depolarization-dependent survival. Thus, survival of SGNs under depolarizing conditions involves additivity among a depolarization-independent autocrine pathway, a cAMP-dependent pathway, and a CaMK-dependent pathway.

Indexed as

AnimalsAutocrine CommunicationCells, CulturedCell SurvivalCyclic AMPMembrane PotentialsRatsSignal TransductionSpiral GanglionCyclic AMP

Identifiers

PMID11264301
PMCPMC6762385
OpenAlexW1675685854

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.