Evidence map›Paper›PMID 23345207›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Distal dendritic inputs control neuronal activity by heterosynaptic potentiation of proximal inputs.

Edward B Han, Stephen F Heinemann

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Heterosynaptic plasticity-induced modulation of synapses.The journal of physiological sciences : JPS · 2023
    Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Increased thin-spine density in frontal cortex pyramidal neurons in a genetic rat model of schizophrenia-relevant features.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2021
    Article
  10. Distance-dependent regulation of NMDAR nanoscale organization along hippocampal neuron dendrites.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. 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

2 authors.

Edward B HanSalk Institute for Biological Studies, La Jolla, California 92037, USA. edbhan@gmail.com
Stephen F Heinemann

Funding

TRAINING IN THE NEUROPLASTICITY OF AGINGT32AG000216 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI KOO, EDWARD H. · 1992 to 2017
$8.4M
Project-002P30NS076411 · NINDS · SCINTILLON INSTITUTE FOR PHOTOBIOLOGY · PI LIPTON, STUART A · 2011 to 2016
$4.5M
NIA NIH HHS T32 AG000216NINDS NIH HHS P30 NS076411
6 · The paper itself

Abstract

Synapses onto distal dendritic tufts are believed to function by modulating time-locked proximal inputs; however, the role of these synapses when proximal inputs are asynchronous or silent is unknown. Surprisingly, we found that activation of apical tuft synapses alone resulted in heterosynaptic potentiation of proximal synapses. In mouse adult hippocampal CA1 pyramidal neurons, we show that activation of distal inputs from the entorhinal cortex (EC) specifically strengthens proximal synapses projecting from CA3. This slow AMPA receptor-mediated potentiation is accompanied by increased synaptic GluN2B-containing NMDA receptors, which are normally restricted to juvenile animals. These two synaptic modifications interact to generate striking bidirectional metaplastic changes. Heterosynaptically potentiated synapses become resistant to subsequent long-term potentiation (LTP) as the two forms of AMPA receptor-mediated potentiation occlude. However, this is only true when the LTP induction protocol is relatively weak. When it is strong and repeated, the magnitude of LTP after heterosynaptic plasticity is greatly increased, specifically through the activation of GluN2B-containing NMDA receptors. Thus, CA1 neurons expressing heterosynaptic potentiation induced by external sensory input from the EC become more strongly driven by internally generated environmental representations from CA3. Furthermore, subsequent SC LTP in this ensemble is shifted to potentiate only strongly activated CA3 inputs, while endowing these synapses with enhanced potentiation. These results show that one set of inputs can exert long-lasting heterosynaptic control over another, allowing the coupling of two functionally and spatially distinct pathways, thereby greatly expanding the repertoire of cellular and network plasticity.

Indexed as

AnimalsCA1 Region, HippocampalDendritesExcitatory Postsynaptic PotentialsLong-Term PotentiationMaleMiceMice, Inbred C57BLNeural PathwaysOrgan Culture TechniquesPatch-Clamp TechniquesPyramidal CellsSynapsesSynaptic Transmission

Identifiers

PMID23345207
PMCPMC3711602

What OpenQuestion holds

Textmetadata
LicenceTDM
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.