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The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss

Overview of attention for article published in Frontiers in Neuroanatomy, February 2017
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Title
The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss
Published in
Frontiers in Neuroanatomy, February 2017
DOI 10.3389/fnana.2017.00009
Pubmed ID
Authors

Verónica Fuentes-Santamaría, Juan Carlos Alvarado, Pedro Melgar-Rojas, María C. Gabaldón-Ull, Josef M. Miller, José M. Juiz

Abstract

Repeated noise exposure induces inflammation and cellular adaptations in the peripheral and central auditory system resulting in pathophysiology of hearing loss. In this study, we analyzed the mechanisms by which noise-induced inflammatory-related events in the cochlea activate glial-mediated cellular responses in the cochlear nucleus (CN), the first relay station of the auditory pathway. The auditory function, glial activation, modifications in gene expression and protein levels of inflammatory mediators and ultrastructural changes in glial-neuronal interactions were assessed in rats exposed to broadband noise (0.5-32 kHz, 118 dB SPL) for 4 h/day during 4 consecutive days to induce long-lasting hearing damage. Noise-exposed rats developed a permanent threshold shift which was associated with hair cell loss and reactive glia. Noise-induced microglial activation peaked in the cochlea between 1 and 10D post-lesion; their activation in the CN was more prolonged reaching maximum levels at 30D post-exposure. RT-PCR analyses of inflammatory-related genes expression in the cochlea demonstrated significant increases in the mRNA expression levels of pro- and anti-inflammatory cytokines, inducible nitric oxide synthase, intercellular adhesion molecule and tissue inhibitor of metalloproteinase-1 at 1 and 10D post-exposure. In noise-exposed cochleae, interleukin-1β (IL-1β), and tumor necrosis factor α (TNF-α) were upregulated by reactive microglia, fibrocytes, and neurons at all time points examined. In the CN, however, neurons were the sole source of these cytokines. These observations suggest that noise exposure causes peripheral and central inflammatory reactions in which TNF-α and IL-1β are implicated in regulating the initiation and progression of noise-induced hearing loss.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 81 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 81 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 15 19%
Student > Master 14 17%
Researcher 12 15%
Professor > Associate Professor 6 7%
Student > Bachelor 5 6%
Other 14 17%
Unknown 15 19%
Readers by discipline Count As %
Neuroscience 25 31%
Agricultural and Biological Sciences 9 11%
Biochemistry, Genetics and Molecular Biology 8 10%
Medicine and Dentistry 7 9%
Engineering 5 6%
Other 9 11%
Unknown 18 22%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 3. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 07 June 2017.
All research outputs
#13,372,881
of 23,295,606 outputs
Outputs from Frontiers in Neuroanatomy
#539
of 1,178 outputs
Outputs of similar age
#156,403
of 311,906 outputs
Outputs of similar age from Frontiers in Neuroanatomy
#16
of 32 outputs
Altmetric has tracked 23,295,606 research outputs across all sources so far. This one is in the 42nd percentile – i.e., 42% of other outputs scored the same or lower than it.
So far Altmetric has tracked 1,178 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.9. This one has gotten more attention than average, scoring higher than 54% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 311,906 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 49th percentile – i.e., 49% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 32 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 53% of its contemporaries.