Evidence map›Paper›PMID 10212287›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999

Brain-derived neurotrophic factor mediates the anti-apoptotic effect of NMDA in cerebellar granule neurons: signal transduction cascades and site of ethanol action.

S V Bhave, L Ghoda, P L Hoffman

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

74 citing papers in PubMed, 216 citations in OpenAlex.

  1. Review
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  6. Article
  7. Effect of Water and Ethanol Extracts fromMolecules (Basel, Switzerland) · 2021
    Article
  8. Symptomatologic pathomechanism ofEncephalitis (Seoul, Korea) · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Visual Experience Facilitates BDNF-Dependent Adaptive Recruitment of New Neurons in the Postembryonic Optic Tectum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  14. Review
  15. Article
  16. Article
  17. Article
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  19. Article
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14 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

S V BhaveDepartment of Pharmacology, University of Colorado Health Sciences Center, Denver, Colorado 80262, USA.
L Ghoda
P L Hoffman
University of Colorado Health · USUniversity of Colorado Anschutz Medical Campus · US

Funding

TRANSGENIC MOUSE MODELS TO STUDY THE ROLE OF NEUROTENSIN RECEPTORP50AA003527 · NIAAA · UNIVERSITY OF COLORADO DENVER · PI DEITRICH, RICHARD A · 1985 to 2003
$5.9M
NMDA RECEPTOR FUNCTION IN ETHANOL WITHDRAWALR01AA009005 · NIAAA · UNIVERSITY OF COLORADO DENVER · PI HOFFMAN, PAULA · 1991 to 2000
$235k
NIAAA NIH HHS AA3527NIAAA NIH HHS AA9005
6 · The paper itself

Abstract

Cerebellar granule neurons cultured in medium containing a physiological concentration of KCl (5 mM) undergo apoptosis. The cells can be rescued by the in vitro addition of NMDA. The protective effect of NMDA is thought to reflect the in vivo innervation of developing cerebellar granule neurons by glutamatergic afferents. In the current work, we investigated the mechanism of the anti-apoptotic (protective) effect of NMDA. NMDA treatment reduced caspase-3-like activity in cerebellar granule neurons, and the time course and concentration dependence of the protective effect of NMDA mirrored the ability of NMDA to induce brain-derived neurotrophic factor (BDNF) expression. Furthermore, a Trk receptor antagonist, K252a, as well as a blocking antibody to BDNF, attenuated the protective effects of both NMDA and BDNF. These results suggest that NMDA-induced BDNF expression mediates the anti-apoptotic effect of NMDA. The protective effects of NMDA and BDNF were reduced by inhibitors of the phosphatidylinositol 3'-OH kinase (PI 3-kinase) signal transduction cascade (wortmannin and LY29004) but not by a MAP kinase kinase (MEK) inhibitor (PD98059) or a protein kinase A inhibitor (Rp-cAMPS). BDNF increased phosphorylation of Akt, a target of PI 3-kinase, and NMDA also induced Akt phosphorylation, but only after an exposure that was long enough to induce BDNF expression. Furthermore, ethanol, which interferes with NMDA receptor function, inhibited the NMDA-induced increase in BDNF levels but did not block the protective effect of BDNF. These findings further support the role of BDNF in the anti-apoptotic effect of NMDA in cerebellar granule neurons and suggest that the NMDA-BDNF interaction may play a key role in in vivo cerebellar granule neuron development, as well as in the deleterious effects of ethanol on the developing cerebellum.

Indexed as

AnimalsApoptosisBrain-Derived Neurotrophic FactorCarbazolesCaspase 3CaspasesCells, CulturedCerebellumChromonesEnzyme InhibitorsEthanolIndole AlkaloidsInsulin-Like Growth Factor IMorpholinesNeuronsNeuroprotective Agents2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-oneBrain-Derived Neurotrophic FactorCarbazolesCasp3 protein, ratCaspase 3CaspasesChromonesEnzyme InhibitorsEthanolIndole AlkaloidsInsulin-Like Growth Factor IMorpholinesNeuroprotective AgentsN-Methylaspartatestaurosporine aglycone

Identifiers

PMID10212287
PMCPMC6782254
OpenAlexW1934034828

What Socratic 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 Socratic graph.