Evidence map›Paper›PMID 22484482›Full record

ArticleNeurobiology of disease2012

Functional alterations in GABAergic fast-spiking interneurons in chronically injured epileptogenic neocortex.

Yunyong Ma, David A Prince

Abstract read
In one paragraph

Article in Neurobiology of disease, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

  1. Internal and external validation of comprehensive high-frequency activity biomarkers for epilepsy surgery.Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
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  10. Review
  11. Article
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  14. From Molecular Circuit Dysfunction to Disease: Case Studies in Epilepsy, Traumatic Brain Injury, and Alzheimer's Disease.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016
    Review
  15. More Docked Vesicles and Larger Active Zones at Basket Cell-to-Granule Cell Synapses in a Rat Model of Temporal Lobe Epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016
    Article
  16. Review
  17. Article
  18. Article
  19. Article
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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

2 authors.

Yunyong MaDept. of Neurology and Neurological Sciences, Stanford University School of Medicine, Stanford, CA 94305-5122, USA.
David A Prince

Funding

REGULATION OF NEURONAL EXCITABILITY IN CHRONIC EPILEPTOGENESISP50NS012151 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1985 to 2007
$9.1M
CELLULAR MECHANISMS IN FOCAL EPILEPTOGENESISR01NS006477 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 1985 to 2013
$5.0M
Epilepsy Research ProgramP01NS012151 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R · 2008 to 2011
$4.4M
MODULATION OF NEOCORTICAL INTERNEURONAL FUNCTIONR01NS039579 · NINDS · STANFORD UNIVERSITY · PI HUGUENARD, JOHN R, PRINCE, DAVID ALLAN · 2000 to 2013
$4.3M
Modulation of Neocortical Interneuronal FunctionR56NS039579 · NINDS · STANFORD UNIVERSITY · PI PRINCE, DAVID ALLAN · 2014 to 2014
$402k
NINDS NIH HHS NS012151NINDS NIH HHS NS039579NINDS NIH HHS P01 NS012151NINDS NIH HHS P50 NS012151NINDS NIH HHS R01 NS006477NINDS NIH HHS R01 NS039579NINDS NIH HHS R56 NS039579
6 · The paper itself

Abstract

Progress toward developing effective prophylaxis and treatment of posttraumatic epilepsy depends on a detailed understanding of the basic underlying mechanisms. One important factor contributing to epileptogenesis is decreased efficacy of GABAergic inhibition. Here we tested the hypothesis that the output of neocortical fast-spiking (FS) interneurons onto postsynaptic targets would be decreased in the undercut (UC) model of chronic posttraumatic epileptogenesis. Using dual whole-cell recordings in layer IV barrel cortex, we found a marked increase in the failure rate and a very large reduction in the amplitude of unitary inhibitory postsynaptic currents (uIPSCs) from FS cells to excitatory regular spiking (RS) neurons and neighboring FS cells. Assessment of the paired pulse ratio and presumed quantal release showed that there was a significant, but relatively modest, decrease in synaptic release probability and a non-significant reduction in quantal size. A reduced density of boutons on axons of biocytin-filled UC FS cells, together with a higher coefficient of variation of uIPSC amplitude in RS cells, suggested that the number of functional synapses presynaptically formed by FS cells may be reduced. Given the marked reduction in synaptic strength, other defects in the presynaptic vesicle release machinery likely occur, as well.

Indexed as

AnimalsAxonsDisease Models, AnimalElectroencephalographyEpilepsy, Post-TraumaticGABAergic NeuronsInhibitory Postsynaptic PotentialsInterneuronsMaleNeocortexNeural InhibitionPatch-Clamp TechniquesPresynaptic TerminalsRatsRats, Sprague-DawleySynaptic Transmission

Identifiers

PMID22484482
PMCPMC3416869

What OpenQuestion holds

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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.