Evidence map›Paper›PMID 11150327›Full record

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

Expression of brain-derived neurotrophic factor in cortical neurons is regulated by striatal target area.

J M Canals, N Checa, S Marco, P Akerud, A Michels, E Pérez-Navarro, E Tolosa, E Arenas, J Alberch

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 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.2field-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

25 citing papers in PubMed, 110 citations in OpenAlex.

  1. Article
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  5. Autophagy and apoptosis cascade: which is more prominent in neuronal death?Cellular and molecular life sciences : CMLS · 2021
    Review
  6. Article
  7. BDNF Expression in Cortical GABAergic Interneurons.International journal of molecular sciences · 2020
    Article
  8. Article
  9. Astrocyte-derived BDNF supports myelin protein synthesis after cuprizone-induced demyelination.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014
    Article
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  11. Article
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  15. Article
  16. Review
  17. Review
  18. Neural transplants in patients with Huntington's disease undergo disease-like neuronal degeneration.Proceedings of the National Academy of Sciences of the United States of America · 2009
    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

9 authors at 2 institutions in 2 countries.

J M CanalsDepartament de Biologia Cel.lular i Anatomia Patològica, Facultat de Medicina, Universitat de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Casanova 143, E-08036 Barcelona, Spain.
N Checa
S Marco
P Akerud
A Michels
E Pérez-Navarro
E Tolosa
E Arenas
J Alberch
Karolinska Institutet · SEUniversitat de Barcelona · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Changes in BDNF expression after different types of brain insults are related to neuroprotection, stimulation of sprouting, and synaptic reorganization. In the cerebral cortex, an autocrine-paracrine mechanism for BDNF has been proposed because the distribution patterns of BDNF and TrkB expression are almost identical. Moreover, cortical BDNF is anterogradely transported to the striatum, suggesting a role of BDNF in the functional interaction between the two brain regions. Here we have examined the expression of this neurotrophin in the cerebral cortex after various striatal lesions. Intrastriatal injection of quinolinate, kainate, 3-nitropropionic acid, or colchicine increased BDNF mRNA levels in cerebral cortex. In contrast, stimulation of neuronal activity in the striatum did not change cortical BDNF expression. Both excitatory amino acids increased BDNF expression in neurons of cortical layers II/III, V, and VI that project to the striatum. Moreover, grafting a BDNF-secreting cell line prevented both the loss of striatal neurons and the cortical upregulation of BDNF induced by excitotoxins. Because retrograde transport in the corticostriatal pathway was intact after striatal lesions, our results suggest that striatal damage upregulates endogenous BDNF in corticostriatal neurons by a transneuronal mechanism, which may constitute a protective mechanism for striatal and/or cortical cells.

Indexed as

Stilbamidines3T3 CellsAnimalsAxonal TransportBrain-Derived Neurotrophic FactorCerebral CortexColchicineCorpus StriatumDisease Models, AnimalFibroblastsFluorescent DyesHippocampusHuntington DiseaseIn Situ HybridizationKainic AcidMale2-hydroxy-4,4'-diamidinostilbene, methanesulfonate salt3-nitropropionic acidBrain-Derived Neurotrophic FactorColchicineFluorescent DyesKainic AcidNitro CompoundsPropionatesQuinolinic AcidRNA, MessengerStilbamidines

Identifiers

PMID11150327
PMCPMC6762434
OpenAlexW1576672022

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.