Evidence map›Paper›PMID 18059328›Full record

ReviewBritish journal of pharmacology2008

Role of the brain-derived neurotrophic factor at glutamatergic synapses.

A L Carvalho, M V Caldeira, S D Santos, C B Duarte

Open access · bronzeAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
123citing papers in PubMed, 4 pooled it
6.3field-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

123 citing papers in PubMed, 4 syntheses or guidelines pooled it, 288 citations in OpenAlex.

  1. Pooled it
  2. The brain-derived neurotrophic-factor (BDNF) val66met polymorphism is associated with geriatric depression: a meta-analysis.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2012
    Pooled it
  3. Pooled it
  4. BDNF Val66Met is associated with introversion and interacts with 5-HTTLPR to influence neuroticism.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2010
    Pooled it
  5. Article
  6. Review
  7. Identification of a neural basis for anorexia nervosa.bioRxiv : the preprint server for biology · 2026
    Article
  8. Toward an NGF-based therapy for Rett syndrome.Frontiers in neuroscience · 2026
    Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Neurobiological Mechanisms of Cognitive Decline Correlated with Brain Aging.Advances in experimental medicine and biology · 2023
    Article
  18. Article
  19. Review
  20. Article

63 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

4 authors at 1 institution in 1 country.

A L CarvalhoCenter for Neuroscience and Cell Biology, Department of Zoology, University of Coimbra, Coimbra, Portugal. alc@ibili.uc.pt
M V Caldeira
S D Santos
C B Duarte
University of Coimbra · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The neurotrophin brain-derived neurotrophic factor (BDNF) plays an important role in the activity-dependent regulation of synaptic structure and function, particularly of the glutamatergic synapses. BDNF may be released in the mature form, which activates preferentially TrkB receptors, or as proBDNF, which is coupled to the stimulation of the p75(NTR). In the mature form BDNF induces rapid effects on glutamate release, and may induce short- and long-term effects on the postsynaptic response to the neurotransmitter. BDNF may affect glutamate receptor activity by inducing the phosphorylation of the receptor subunits, which may also affect the interaction with intracellular proteins and, consequently, their recycling and localization to defined postsynaptic sites. Stimulation of the local protein synthesis and transcription activity account for the delayed effects of BDNF on glutamatergic synaptic strength. Several evidences show impaired synaptic plasticity of glutamatergic synapses in diseases where compromised BDNF function has been observed, such as Huntington's disease, depression, anxiety, and the BDNF polymorphism Val66Met, suggesting that upregulating BDNF-activated pathways may be therapeutically relevant. This review focuses on recent advances in the understanding of the regulation of the glutamatergic synapse by BDNF, and its implications in synaptic plasticity.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorGlutamic AcidHumansNeuronal PlasticityReceptor, Nerve Growth FactorReceptor, trkBSignal TransductionSubcellular FractionsSynapsesBrain-Derived Neurotrophic FactorGlutamic AcidReceptor, Nerve Growth FactorReceptor, trkB

Identifiers

PMID18059328
PMCPMC2268077
OpenAlexW2100344731

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.