Evidence map›Paper›PMID 15175384›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004

A novel mechanism for the facilitation of theta-induced long-term potentiation by brain-derived neurotrophic factor.

Enikö A Kramár, Bin Lin, Ching-Yi Lin, Amy C Arai, Christine M Gall, Gary Lynch

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
4.7field-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

96 citing papers in PubMed, 173 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. BK channels sustain neuronal CaCellular and molecular life sciences : CMLS · 2023
    Article
  6. Article
  7. Article
  8. BDNF Therapeutic Mechanisms in Neuropsychiatric Disorders.International journal of molecular sciences · 2022
    Review
  9. Article
  10. Article
  11. Frontiers in pharmacology · 2021
    Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Learning and aging affect neuronal excitability and learning.Neurobiology of learning and memory · 2020
    Review
  18. Senescent neurophysiology: CaNeurobiology of learning and memory · 2019
    Review
  19. Review
  20. Article

36 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

6 authors at 2 institutions in 1 country.

Enikö A KramárDepartment of Psychiatry and Human Behavior, University of California, Irvine, California 92612-1695, USA. ekramar@uci.edu
Bin Lin
Ching-Yi Lin
Amy C Arai
Christine M Gall
Gary Lynch
University of California, Irvine · USSouthern Illinois University School of Medicine · US

Funding

The Spine Cytoskeleton and Memory DisordersP01NS045260 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI GALL, CHRISTINE M · 2003 to 2015
$14.4M
NINDS NIH HHS NS045260NINDS NIH HHS P01 NS045260
6 · The paper itself

Abstract

Brain-derived neurotrophic factor (BDNF) contributes to the induction of long-term potentiation (LTP) by theta-pattern stimulation, but the specific processes underlying this effect are not known. Experiments described here, using BDNF concentrations that have minor effects on baseline responses, show that the neurotrophin both reduces the threshold for LTP induction and elevates the ceiling on maximal potentiation. The enhanced LTP proved to be as stable and resistant to reversal as that recorded under control conditions. BDNF markedly increased the facilitation of burst responses that occurs within a theta train. This suggests that the neurotrophin acts on long-lasting events that (1) are set in motion by the first burst in a train and (2) regulate the amplitude of subsequent bursts. Whole-cell recordings established that BDNF causes a rapid reduction in the size of the long-lasting afterhyperpolarization (AHP) that follows individual theta bursts. Apamin, an antagonist of type 2 small-conductance Ca2+-activated potassium (SK2) channels, also reduced hippocampal AHPs and closely reproduced the effects of BDNF on theta-burst responses and LTP. The latter results were replicated with a newly introduced, highly selective inhibitor of SK2 channels. Immunoblot analyses indicated that BDNF increases SK2 serine phosphorylation in hippocampal slices. These findings point to the conclusion that BDNF-driven protein kinase cascades serve to depress the SK2 component, and possibly other constituents, of the AHP. It is likely that this mechanism, acting with other factors, promotes the formation and increases the magnitude of LTP.

Indexed as

Potassium Channels, Calcium-ActivatedAnimalsApaminBrain-Derived Neurotrophic FactorCalciumDose-Response Relationship, DrugElectric StimulationExcitatory Postsynaptic PotentialsHippocampusIn Vitro TechniquesLong-Term PotentiationMalePatch-Clamp TechniquesPhosphorylationPotassium Channel BlockersPotassium ChannelsApaminBrain-Derived Neurotrophic FactorCalciumKcnn2 protein, ratPotassium Channel BlockersPotassium ChannelsPotassium Channels, Calcium-ActivatedSmall-Conductance Calcium-Activated Potassium Channels

Identifiers

PMID15175384
PMCPMC6729196
OpenAlexW2111070504

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.