Evidence map›Paper›PMID 9952419›Full record

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

Selective inhibition of kindling development by intraventricular administration of TrkB receptor body.

D K Binder, M J Routbort, T E Ryan, G D Yancopoulos, J O McNamara

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 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
4.1field-weighted citation impact, top 4% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Low-dose 7,8-Dihydroxyflavone Administration After Status Epilepticus Prevents Epilepsy Development.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2022
    Article
  6. Article
  7. Insights into Potential Targets for Therapeutic Intervention in Epilepsy.International journal of molecular sciences · 2020
    Review
  8. COX-2/PGEEpilepsia open · 2020
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Novel therapeutic approaches for disease-modification of epileptogenesis for curing epilepsy.Biochimica et biophysica acta. Molecular basis of disease · 2017
    Review
  17. Article
  18. Article
  19. Article
  20. Article

1 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

5 authors at 3 institutions in 2 countries.

D K BinderDepartment of Neurobiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
M J Routbort
T E Ryan
G D Yancopoulos
J O McNamara
Institute of Neurobiology · BGRegeneron (United States) · USDuke Medical Center · US

Funding

SYNAPTIC COMPONENTS OF EPILEPTIFORM BURSTSP01NS017771 · NINDS · DUKE UNIVERSITY · PI MCNAMARA, JAMES O. · 1985 to 2004
$7.1M
NINDS NIH HHS NS-17771NINDS NIH HHS P01 NS017771
6 · The paper itself

Abstract

Recent work has shown that neurotrophin gene expression is increased after seizures evoked in the kindling model of epilepsy, but whether neurotrophins regulate kindling development is as yet unclear. In this study, we attempted to block selectively the activation of distinct neurotrophin receptors throughout kindling development in the rat via chronic intracerebroventricular administration of trk receptor bodies. The efficacy and selectivity of the trk receptor bodies were established by inhibition of neurotrophin-induced trk receptor phosphorylation in pheochromocytoma (PC12) cells and primary cultures of cortical neurons. The intracerebroventricular infusion of trkB receptor body (trkB-Fc) inhibited development of kindling in comparison with that seen with saline or human IgG controls, trkA-Fc, or trkC-Fc. These results imply that activation of trkB receptors contributes to the development of kindling, a form of activity-dependent behavioral plasticity in the adult mammalian brain.

Indexed as

Receptor Protein-Tyrosine KinasesReceptors, Nerve Growth FactorAnimalsBaculoviridaeBlotting, WesternElectrodes, ImplantedImmunohistochemistryInjections, IntraventricularKindling, NeurologicMaleNeuroprotective AgentsRatsRats, Sprague-DawleyReceptor, Ciliary Neurotrophic FactorNeuroprotective AgentsReceptor, Ciliary Neurotrophic FactorReceptor Protein-Tyrosine KinasesReceptors, Nerve Growth Factor

Identifiers

PMID9952419
PMCPMC6786043
OpenAlexW1942924653

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.