Evidence map›Paper›PMID 22773781›Full record

ArticleJournal of neurophysiology2012

Decreased afferent excitability contributes to synaptic depression during high-frequency stimulation in hippocampal area CA1.

Eunyoung Kim, Benjamin Owen, William R Holmes, Lawrence M Grover

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

22 citing papers in PubMed, 44 citations in OpenAlex.

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  10. Anticonvulsant vs. Proconvulsant Effect ofFrontiers in systems neuroscience · 2021
    Article
  11. Ultrafast glutamate sensors resolve high-frequency release at Schaffer collateral synapses.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  12. Article
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  16. Energy and Potassium Ion Homeostasis during Gamma Oscillations.Frontiers in molecular neuroscience · 2016
    Review
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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 2 institutions in 1 country.

Eunyoung KimDepartment of Pharmacology, Physiology, and Toxicology, Marshall University, School of Medicine, Huntington, West Virginia 25755, USA.
Benjamin Owen
William R Holmes
Lawrence M Grover
Marshall University · USOhio University · US

Funding

Models of Signaling Mechanisms in LTPR01AA014294 · NIAAA · OHIO UNIVERSITY ATHENS · PI HOLMES, WILLIAM R · 2002 to 2006
$1.1M
NIAAA NIH HHS AA-014294
6 · The paper itself

Abstract

Long-term potentiation (LTP) is often induced experimentally by continuous high-frequency afferent stimulation (HFS), typically at 100 Hz for 1 s. Induction of LTP requires postsynaptic depolarization and voltage-dependent calcium influx. Induction is more effective if the same number of stimuli are given as a series of short bursts rather than as continuous HFS, in part because excitatory postsynaptic potentials (EPSPs) become strongly depressed during HFS, reducing postsynaptic depolarization. In this study, we examined mechanisms of EPSP depression during HFS in area CA1 of rat hippocampal brain slices. We tested for presynaptic terminal vesicle depletion by examining minimal stimulation-evoked excitatory postsynaptic currents (EPSCs) during 100-Hz HFS. While transmission failures increased, consistent with vesicle depletion, EPSC latencies also increased during HFS, suggesting a decrease in afferent excitability. Extracellular recordings of Schaffer collateral fiber volleys confirmed a decrease in afferent excitability, with decreased fiber volley amplitudes and increased latencies during HFS. To determine the mechanism responsible for fiber volley changes, we recorded antidromic action potentials in single CA3 pyramidal neurons evoked by stimulating Schaffer collateral axons. During HFS, individual action potentials decreased in amplitude and increased in latency, and these changes were accompanied by a large increase in the probability of action potential failure. Time derivative and phase-plane analyses indicated decreases in both axon initial segment and somato-dendritic components of CA3 neuron action potentials. Our results indicate that decreased presynaptic axon excitability contributes to depression of excitatory synaptic transmission during HFS at synapses between Schaffer collaterals and CA1 pyramidal neurons.

Indexed as

Excitatory Postsynaptic PotentialsAction PotentialsAfferent PathwaysAnimalsCA1 Region, HippocampalCA3 Region, HippocampalCalciumElectric StimulationLong-Term Synaptic DepressionMalePyramidal CellsRatsRats, Sprague-DawleySynaptic VesiclesCalcium

Identifiers

PMID22773781
PMCPMC3544996
OpenAlexW2025462332

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.