Evidence map›Paper›PMID 19171653›Full record

ArticleThe Journal of physiology2009

Activity-dependent depression of the spike after-depolarization generates long-lasting intrinsic plasticity in hippocampal CA3 pyramidal neurons.

Jon T Brown, Andrew D Randall

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

45 citing papers in PubMed, 73 citations in OpenAlex.

  1. Trial
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  6. Adam, amigo, brain, and K channel.Biophysical reviews · 2023
    Review
  7. Cholinergic Stimulation Modulates the Functional Composition of CA3 Cell Types in the Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  8. Article
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  12. The subthreshold-active KCommunications biology · 2019
    Article
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  15. Review
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  20. Learning Universal Computations with Spikes.PLoS computational biology · 2016
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Jon T BrownMRC Centre for Synaptic Plasticity, Department of Anatomy, University of Bristol, University Walk, Bristol BS8 1TD, UK. jon.brown@bristol.ac.uk
Andrew D Randall
University of Bristol · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent plastic changes to the intrinsic excitability of neurons have substantial implications for computational processing within the CNS. We have identified and characterized a novel long-lasting form of intrinsic plasticity in hippocampal CA3 pyramidal cells. Although the patterns of action potential firing elicited in this cell population by depolarizing current injections exhibited considerable diversity, practically all cells produced an initial high frequency (>100 Hz) burst of two to five spikes. This burst involved conductances that were responsible for the prominent spike afterdepolarization of CA3 pyramids. Long-lasting changes in the firing behaviour of CA3 cells were produced by conditioning stimuli (CS) consisting of either periods of depolarization in voltage clamp or periods of short (2 or 4 spikes) high frequency (circa 100 Hz) burst firing at 5 or 10 Hz. CS-induced changes included substantial prolongation of the first inter-spike interval and increased spike jitter. Similar CS-induced changes were seen when the test stimulus used to elicit firing resembled a glutamatergic EPSC. In line with this, a long-lasting depression of the ADP was elicited by the same CS that altered firing patterns of CA3 cells. Conditioning-induced changes in both spiking patterns and ADP amplitude were blocked by buffering intracellular Ca(2+) with BAPTA. Furthermore, the Kv7 channel blocker XE991, a cognitive enhancer, both enhanced the ADP and completely eliminated its conditioning-induced depression. These findings indicate that a persistent enhancement of Kv7 channels, following a transient increase in cytoplasmic Ca(2+), results in a prolonged depression of the ADP in CA3 pyramidal neurones.

Indexed as

Action PotentialsAnimalsAnthracenesCalcium Channel AgonistsCalcium Channel BlockersCalcium SignalingCarbamatesCardiovascular AgentsChelating AgentsEgtazic AcidHippocampusIn Vitro TechniquesKCNQ Potassium ChannelsMaleMembrane PotentialsNeuronal Plasticity10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acidAnthracenesCalcium Channel AgonistsCalcium Channel BlockersCarbamatesCardiovascular AgentsChelating AgentsEgtazic AcidezogabineICI D2788KCNQ Potassium ChannelsPhenylenediaminesPyrimidines

Identifiers

PMID19171653
PMCPMC2674996
OpenAlexW2134610645

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.