Evidence map›Paper›PMID 21957228›Full record

ArticleJournal of neurophysiology2012

Plasticity of spontaneous excitatory and inhibitory synaptic activity in morphologically defined vestibular nuclei neurons during early vestibular compensation.

Mei Shao, June C Hirsch, Kenna D Peusner

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 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing 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

15 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. The two faces of synaptic failure in AppAlzheimer's research & therapy · 2020
    Article
  7. A New Model for Congenital Vestibular Disorders.Journal of the Association for Research in Otolaryngology : JARO · 2019
    Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. 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.

Mei ShaoDept. of Anatomy and Regenerative Biology, George Washington Univ. Medical Center, 2300 I St. N.W., Washington, DC 20037, USA. anakdp@gwumc.edu
June C Hirsch
Kenna D Peusner

Funding

SYNAPTIC TRANSMISSION DURING NEURONAL DIFFERENTIATIONR01DC000970 · NIDCD · GEORGE WASHINGTON UNIVERSITY · PI PEUSNER, KENNA D · 1991 to 2010
$4.2M
Acquisition of Zeiss 710 Confocal Laser Scanning MicroscopeS10RR025565 · NCRR · GEORGE WASHINGTON UNIVERSITY · PI POPRATILOFF, ANASTAS · 2009 to 2009
$500k
NCRR NIH HHS S10-RR-025565NIDCD NIH HHS R01-DC-000970
6 · The paper itself

Abstract

After unilateral peripheral vestibular lesions, the brain plasticity underlying early recovery from the static symptoms is not fully understood. Principal cells of the chick tangential nucleus offer a subset of morphologically defined vestibular nuclei neurons to study functional changes after vestibular lesions. Chickens show posture and balance deficits immediately after unilateral vestibular ganglionectomy (UVG), but by 3 days most subjects begin to recover, although some remain uncompensated. With the use of whole cell voltage-clamp, spontaneous excitatory and inhibitory postsynaptic currents (sEPSCs and sIPSCs) and miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs) were recorded from principal cells in brain slices 1 and 3 days after UVG. One day after UVG, sEPSC frequency increased on the lesion side and remained elevated at 3 days in uncompensated chickens only. Also by 3 days, sIPSC frequency increased on the lesion side in all operated chickens due to major increases in GABAergic events. Significant change also occurred in decay time of the events. To determine whether fluctuations in frequency and kinetics influenced overall excitatory or inhibitory synaptic drive, synaptic charge transfer was calculated. Principal cells showed significant increase in excitatory synaptic charge transfer only on the lesion side of uncompensated chickens. Thus compensation continues when synaptic charge transfer is in balance bilaterally. Furthermore, excessive excitatory drive in principal cells on the lesion side may prevent vestibular compensation. Altogether, this work is important for it defines the time course and excitatory and inhibitory nature of changing spontaneous synaptic inputs to a morphologically defined subset of vestibular nuclei neurons during critical early stages of recovery after UVG.

Indexed as

AnimalsAnimals, NewbornChickensExcitatory Postsynaptic PotentialsInhibitory Postsynaptic PotentialsNeural InhibitionNeuronal PlasticityNeuronsSynaptic TransmissionVestibular Nuclei

Identifiers

PMID21957228
PMCPMC3349683

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.