Evidence map›Paper›PMID 19692507›Full record

ArticleJournal of neurophysiology2009

Balance of inhibitory and excitatory synaptic activity is altered in fast-spiking interneurons in experimental cortical dysplasia.

Fu-Wen Zhou, Huan-Xin Chen, Steven N Roper

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
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  4. Article
  5. PostnataliScience · 2021
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  19. Review
  20. Cortical dysplasia: a possible substrate for brain tumors.Future oncology (London, England) · 2012
    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 at 1 institution in 1 country.

Fu-Wen ZhouDepartment of Neurosurgery and the McKnight Brain Institute, University of Florida, Gainesville, Florida 32610, USA.
Huan-Xin Chen
Steven N Roper
University of Florida · US

Funding

Disorders of Neuronal Migration and EpilepsyR01NS035651 · NINDS · UNIVERSITY OF FLORIDA · PI ROPER, STEVEN N · 2003 to 2005
$605k
DISORDERS OF NEURONAL MIGRATION AND EPILEPSYR29NS035651 · NINDS · UNIVERSITY OF FLORIDA · PI ROPER, STEVEN N · 1998 to 2002
$303k
NINDS NIH HHS NS-35651NINDS NIH HHS R01 NS035651NINDS NIH HHS R29 NS035651
6 · The paper itself

Abstract

Cortical dysplasia (CD) is a common cause of intractable epilepsy in children and adults. We have studied rats irradiated in utero as a model of CD to better understand mechanisms that underlie dysplasia-associated epilepsy. Prior studies have shown a reduction in the number of cortical interneurons and in the frequency of inhibitory postsynaptic currents (IPSCs) in pyramidal cells in this model. They have also shown a reduced frequency of spontaneous and miniature excitatory postsynaptic currents (EPSCs) in the surviving cortical interneurons. However, the inhibitory synaptic contacts were not examined in that study. The current experiments were performed to assess inhibitory synaptic activity in fast-spiking (FS) interneurons in irradiated rats and controls and the balance of excitatory and inhibitory synaptic activity in these cells. Whole cell recordings were obtained from layer IV FS cells in controls and comparable FS cells in irradiated rats. The frequency of spontaneous and miniature IPSCs was reduced in dysplastic cortex, but the amplitude of these currents was unchanged. Stimulus-evoked IPSCs showed short-term depression in control and short-term facilitation in dysplastic cortex. Simultaneous recording of spontaneous EPSCs and IPSCs showed a shift in the ratio of excitation-to-inhibition in favor of inhibition in FS cells from dysplastic cortex. The same shift toward inhibition was seen when miniature EPSCs and IPSCs were examined. These results show that FS cells in dysplastic cortex have a relative lack of excitatory drive. This may result in an important class of inhibitory cells that are less able to perform their normal function especially in periods of increased excitatory activity.

Indexed as

Action PotentialsAnimalsCerebral CortexExcitatory Postsynaptic PotentialsInhibitory Postsynaptic PotentialsInterneuronsIn Vitro TechniquesMaleMalformations of Cortical DevelopmentNeural InhibitionNeuronal PlasticityParvalbuminsRadiation Injuries, ExperimentalRatsRats, Sprague-DawleySynapsesParvalbumins

Identifiers

PMID19692507
PMCPMC2775391
OpenAlexW2135227965

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.