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Acute Noise Exposure Is Associated With Intrinsic Apoptosis in Murine Central Auditory Pathway

Overview of attention for article published in Frontiers in Neuroscience, May 2018
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Title
Acute Noise Exposure Is Associated With Intrinsic Apoptosis in Murine Central Auditory Pathway
Published in
Frontiers in Neuroscience, May 2018
DOI 10.3389/fnins.2018.00312
Pubmed ID
Authors

Moritz Gröschel, Dietmar Basta, Arne Ernst, Birgit Mazurek, Agnieszka J. Szczepek

Abstract

Noise that is capable of inducing the hearing loss (NIHL) has a strong impact on the inner ear structures and causes early and most obvious pathophysiological changes in the auditory periphery. Several studies indicated that intrinsic apoptotic cell death mechanisms are the key factors inducing cellular degeneration immediately after noise exposure and are maintained for days or even weeks. In addition, studies demonstrated several changes in the central auditory system following noise exposure, consistent with early apoptosis-related pathologies. To clarify the underlying mechanisms, the present study focused on the noise-induced gene and protein expression of the pro-apoptotic protease activating factor-1 (APAF1) and the anti-apoptotic B-cell lymphoma 2 related protein a1a (BCL2A1A) in the cochlear nucleus (CN), inferior colliculus (IC) and auditory cortex (AC) of the murine central auditory pathway. The expression of Bcl2a1a mRNA was upregulated immediately after trauma in all tissues investigated, whereas the protein levels were significantly reduced at least in the auditory brainstem. Conversely, acute noise has decreased the expression of Apaf1 gene along the auditory pathway. The changes in APAF1 protein level were not statistically significant. It is tempting to speculate that the acoustic overstimulation leads to mitochondrial dysfunction and induction of apoptosis by regulation of proapoptotic and antiapoptotic proteins. The inverse expression pattern on the mRNA level of both genes might reflect a protective response to decrease cellular damage. Our results indicate the immediate presence of intrinsic apoptosis following noise trauma. This, in turn, may significantly contribute to the development of central structural deficits. Auditory pathway-specific inhibition of intrinsic apoptosis could be a therapeutic approach for the treatment of acute (noise-induced) hearing loss to prevent irreversible neuronal injury in auditory brain structures and to avoid profound deficits in complex auditory processing.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 28 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 28 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 7 25%
Student > Bachelor 3 11%
Student > Master 3 11%
Student > Ph. D. Student 3 11%
Professor > Associate Professor 2 7%
Other 2 7%
Unknown 8 29%
Readers by discipline Count As %
Neuroscience 6 21%
Agricultural and Biological Sciences 3 11%
Medicine and Dentistry 3 11%
Biochemistry, Genetics and Molecular Biology 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Other 4 14%
Unknown 9 32%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 2. 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 28 August 2018.
All research outputs
#16,728,456
of 25,382,440 outputs
Outputs from Frontiers in Neuroscience
#7,428
of 11,542 outputs
Outputs of similar age
#209,284
of 341,024 outputs
Outputs of similar age from Frontiers in Neuroscience
#171
of 237 outputs
Altmetric has tracked 25,382,440 research outputs across all sources so far. This one is in the 32nd percentile – i.e., 32% of other outputs scored the same or lower than it.
So far Altmetric has tracked 11,542 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 11.0. This one is in the 31st percentile – i.e., 31% of its peers scored the same or lower than it.
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 341,024 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 35th percentile – i.e., 35% of its contemporaries scored the same or lower than it.
We're also able to compare this research output to 237 others from the same source and published within six weeks on either side of this one. This one is in the 22nd percentile – i.e., 22% of its contemporaries scored the same or lower than it.