Evidence map›Paper›PMID 21106811›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010

Pyramidal neuron conductance state gates spike-timing-dependent plasticity.

Jary Y Delgado, José F Gómez-González, Niraj S Desai

Abstract readComparative Study
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Dynamics of a Mutual Inhibition Circuit between Pyramidal Neurons Compared to Human Perceptual Competition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  5. Hebbian plasticity requires compensatory processes on multiple timescales.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017
    Review
  6. Natural Firing Patterns Imply Low Sensitivity of Synaptic Plasticity to Spike Timing Compared with Firing Rate.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  7. Article
  8. Review
  9. Sloppiness in spontaneously active neuronal networks.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  10. Article
  11. Article
  12. Heterosynaptic plasticity prevents runaway synaptic dynamics.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  13. Article
  14. Synaptic and intrinsic balancing during postnatal development in rat pups exposed to valproic acid in utero.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011
    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

3 authors.

Jary Y DelgadoThe Neurosciences Institute, San Diego, CA 92121, USA.
José F Gómez-González
Niraj S Desai

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neocortical neurons in vivo process each of their individual inputs in the context of ongoing synaptic background activity, produced by the thousands of presynaptic partners a typical neuron has. Previous work has shown that background activity affects multiple aspects of neuronal and network function. However, its effect on the induction of spike-timing dependent plasticity (STDP) is not clear. Here we report that injections of simulated background conductances (produced by a dynamic-clamp system) into pyramidal cells in rat brain slices selectively reduced the magnitude of timing-dependent synaptic potentiation while leaving the magnitude of timing-dependent synaptic depression unchanged. The conductance-dependent suppression also sharpened the STDP curve, with reliable synaptic potentiation induced only when EPSPs and action potentials (APs) were paired within 8 ms of each other. Dual somatic and dendritic patch recordings suggested that the deficit in synaptic potentiation arose from shunting of dendritic EPSPs and APs. Using a biophysically detailed computational model, we were not only able to replicate the conductance-dependent shunting of dendritic potentials, but show that synaptic background can truncate calcium dynamics within dendritic spines in a way that affects potentiation more strongly than depression. This conductance-dependent regulation of synaptic plasticity may constitute a novel homeostatic mechanism that can prevent the runaway synaptic potentiation to which Hebbian networks are vulnerable.

Indexed as

Action PotentialsAnimalsAnimals, NewbornExcitatory Postsynaptic PotentialsNeural ConductionNeuronal PlasticityPyramidal CellsRatsRats, Sprague-DawleySensory GatingSynaptic PotentialsSynaptic TransmissionTime Factors

Identifiers

PMID21106811
PMCPMC6633743

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.