Evidence map›Paper›PMID 24316061›Full record

ArticleNeuroscience2014

Age-related hearing loss: GABA, nicotinic acetylcholine and NMDA receptor expression changes in spiral ganglion neurons of the mouse.

X Tang, X Zhu, B Ding, J P Walton, R D Frisina, J Su

Abstract read
In one paragraph

Article in Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 11% 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

28 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Review
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  11. A review of the auditory-gut-brain axis.Frontiers in neuroscience · 2023
    Review
  12. Article
  13. Article
  14. Planar cell polarity defects and hearing loss in sperm-associated antigen 6 (American journal of physiology. Cell physiology · 2021
    Article
  15. Article
  16. Neurotoxicity of sodium salicylate to the spiral ganglion neurons: GABAJournal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2019
    Article
  17. Article
  18. Article
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

X TangDepartment of Otolaryngology Head and Neck Surgery, First Affiliated Hospital, Guangxi Medical University, 6 Shuangyong Road, Nanning, Guangxi, 530021, China; Department Chemical and Biomedical Engineering, University of South Florida, Tampa, FL 33620, United States; Global Center for Hearing and Speech Research, University of South Florida, Tampa, FL 33620, United States. Electronic address: xiaolan@usf.edu.
X ZhuDepartment Chemical and Biomedical Engineering, University of South Florida, Tampa, FL 33620, United States; Global Center for Hearing and Speech Research, University of South Florida, Tampa, FL 33620, United States. Electronic address: xiaoxiazhu@usf.edu.
B DingDepartment Communication Sciences & Disorders, University of South Florida, Tampa, FL 33620, United States; Global Center for Hearing and Speech Research, University of South Florida, Tampa, FL 33620, United States. Electronic address: ding1@usf.edu.
J P WaltonDepartment Chemical and Biomedical Engineering, University of South Florida, Tampa, FL 33620, United States; Department Communication Sciences & Disorders, University of South Florida, Tampa, FL 33620, United States; Global Center for Hearing and Speech Research, University of South Florida, Tampa, FL 33620, United States. Electronic address: jwalton1@usf.edu.
R D FrisinaDepartment Chemical and Biomedical Engineering, University of South Florida, Tampa, FL 33620, United States; Department Communication Sciences & Disorders, University of South Florida, Tampa, FL 33620, United States; Global Center for Hearing and Speech Research, University of South Florida, Tampa, FL 33620, United States. Electronic address: rfrisina@usf.edu.
J SuDepartment of Otolaryngology Head and Neck Surgery, First Affiliated Hospital, Guangxi Medical University, 6 Shuangyong Road, Nanning, Guangxi, 530021, China. Electronic address: jipingsu@yahoo.com.
University of South Florida · USGuangxi Medical University · CN

Funding

Structure and Function Services CoreP01AG009524 · NIA · UNIVERSITY OF SOUTH FLORIDA · PI FRISINA, ROBERT D · 1992 to 2021
$23.2M
NIA NIH HHS P01 AG009524
6 · The paper itself

Abstract

Age-related hearing loss - presbycusis - is the number one communication disorder and most prevalent neurodegenerative condition of our aged population. Although speech understanding in background noise is quite difficult for those with presbycusis, there are currently no biomedical treatments to prevent, delay or reverse this condition. A better understanding of the cochlear mechanisms underlying presbycusis will help lead to future treatments. Objectives of the present study were to investigate GABAA receptor subunit α1, nicotinic acetylcholine (nACh) receptor subunit β2, and N-methyl-d-aspartate (NMDA) receptor subunit NR1 mRNA and protein expression changes in spiral ganglion neurons (SGN) of the CBA/CaJ mouse cochlea, that occur in age-related hearing loss, utilizing quantitative immunohistochemistry and semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) techniques. We found that auditory brainstem response (ABR) thresholds shifted over 40dB from 3 to 48kHz in old mice compared to young adults. DPOAE thresholds also shifted over 40dB from 6 to 49kHz in old mice, and their amplitudes were significantly decreased or absent in the same frequency range. SGN density decreased with age in basal, middle and apical turns, and SGN density of the basal turn declined the most. A positive correlation was observed between SGN density and ABR wave 1amplitude. mRNA and protein expression of GABAAR α1 and AChR β2 decreased with age in SGNs in the old mouse cochlea. mRNA and protein expression of NMDAR NR1 increased with age in SGNs of the old mice. These findings demonstrate that there are functionally-relevant age-related changes of GABAAR, nAChR, NMDAR expression in CBA mouse SGNs reflecting their degeneration, which may be related to functional changes in cochlear synaptic transmission with age, suggesting biological mechanisms for peripheral age-related hearing loss.

Indexed as

Acoustic StimulationAgingAnalysis of VarianceAnimalsCochleaEvoked Potentials, Auditory, Brain StemMiceMice, Inbred CBANeuronsReceptors, GABA-AReceptors, NicotinicReceptors, N-Methyl-D-AspartateRNA, MessengerSpiral GanglionNR1 NMDA receptorReceptors, GABA-AReceptors, NicotinicReceptors, N-Methyl-D-AspartateRNA, MessengerABRagingauditory brainstem responsecochleadistortion product otoacoustic emissionsDPOAEEDTAethylenediaminetetraacetic acidgene expressionH&Ehearing losshematoxylin and eosinICinferior colliculusnAChnicotinic acetylcholineNMDARN-methyl-d-aspartate receptorOHCouter hair cellsPBSphosphate-buffered salineprotein expressionSGNspiral ganglion neuronspiral ganglion neuronsTDTTucker-Davis technologies

Identifiers

PMID24316061
PMCPMC3935603
OpenAlexW2090101437

What OpenQuestion holds

Textmetadata
LicenceTDM
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.