Evidence map›Paper›PMID 24848470›Full record

ArticleJournal of neurophysiology2014

Long-term deficits in motion detection thresholds and spike count variability after unilateral vestibular lesion.

Xiong-Jie Yu, Jakob S Thomassen, J David Dickman, Shawn D Newlands, Dora E Angelaki

Open access · greenAbstract read
In one paragraph

Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. How Peripheral Vestibular Damage Affects Velocity Storage: a Causative Explanation.Journal of the Association for Research in Otolaryngology : JARO · 2022
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  14. Neuronal thresholds and choice-related activity of otolith afferent fibers during heading perception.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  15. Coding of envelopes by correlated but not single-neuron activity requires neural variability.Proceedings of the National Academy of Sciences of the United States of America · 2015
    Article
  16. 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

5 authors at 2 institutions in 1 country.

Xiong-Jie YuDepartment of Neuroscience, Baylor College of Medicine, Houston, Texas; Department of Anatomy & Neurobiology, Washington University, St. Louis, Missouri; and.
Jakob S ThomassenDepartment of Neuroscience, Baylor College of Medicine, Houston, Texas; Department of Anatomy & Neurobiology, Washington University, St. Louis, Missouri; and.
J David DickmanDepartment of Neuroscience, Baylor College of Medicine, Houston, Texas; Department of Anatomy & Neurobiology, Washington University, St. Louis, Missouri; and.
Shawn D NewlandsDepartment of Otolaryngology, University of Rochester Medical Center, Rochester, New York.
Dora E AngelakiDepartment of Neuroscience, Baylor College of Medicine, Houston, Texas; Department of Anatomy & Neurobiology, Washington University, St. Louis, Missouri; and angelaki@bcm.edu.
Baylor College of Medicine · USUniversity of Rochester Medical Center · US

Funding

NEURAL MECHANISMS OF VESTIBULAR FUNCTIONR01DC004260 · NIDCD · WASHINGTON UNIVERSITY · PI ANGELAKI, DORA · 1999 to 2025
$11.6M
NIDCD NIH HHS DC-04260NIDCD NIH HHS R01 DC004260
6 · The paper itself

Abstract

The vestibular system operates in a push-pull fashion using signals from both labyrinths and an intricate bilateral organization. Unilateral vestibular lesions cause well-characterized motor deficits that are partially compensated over time and whose neural correlates have been traced in the mean response modulation of vestibular nuclei cells. Here we compare both response gains and neural detection thresholds of vestibular nuclei and semicircular canal afferent neurons in intact vs. unilateral-lesioned macaques using three-dimensional rotation and translation stimuli. We found increased stimulus-driven spike count variability and detection thresholds in semicircular canal afferents, although mean responses were unchanged, after contralateral labyrinth lesion. Analysis of trial-by-trial spike count correlations of a limited number of simultaneously recorded pairs of canal afferents suggests increased noise correlations after lesion. In addition, we also found persistent, chronic deficits in rotation detection thresholds of vestibular nuclei neurons, which were larger in the ipsilesional than the contralesional brain stem. These deficits, which persisted several months after lesion, were due to lower rotational response gains, whereas spike count variability was similar in intact and lesioned animals. In contrast to persistent deficits in rotation threshold, translation detection thresholds were not different from those in intact animals. These findings suggest that, after compensation, a single labyrinth is sufficient to recover motion sensitivity and normal thresholds for the otolith, but not the semicircular canal, system.

Indexed as

Evoked Potentials, SomatosensoryMotion PerceptionAnimalsMacaca mulattaMaleNeurons, AfferentRotationSemicircular CanalsSensory ThresholdsVestibular NucleiVestibule, Labyrinthinterneuronal correlationthresholdvariabilityvestibular afferentsvestibular nuclei

Identifiers

PMID24848470
PMCPMC4122753
OpenAlexW1986500941

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.