ArticleNoise & health
Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex.
Article in Noise & health. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Effects of Noise Stress on Neuronal Activation in Rat Auditory Pathway-Related Brain Regions.Diagnostics (Basel, Switzerland) · 2025Article
- Early Loss of Spiral Ganglion Neurons in the Auditory System after Noise Trauma.Audiology & neuro-otology · 2024Article
- Article
- Acute Noise Exposure Is Associated With Intrinsic Apoptosis in Murine Central Auditory Pathway.Frontiers in neuroscience · 2018Article
- Apoptosis in the cochlear nucleus and inferior colliculus upon repeated noise exposure.Noise & healthArticle
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It has previously been shown that acoustic overstimulation induces cell death and extensive cell loss in key structures of the central auditory pathway. A correlation between noise-induced apoptosis and cell loss was hypothesized for the cochlear nucleus and colliculus inferior. To determine the role of cell death in noise-induced cell loss in thalamic and cortical structures, the present mouse study (NMRI strain) describes the time course following noise exposure of cell death mechanisms for the ventral medial geniculate body (vMGB), medial MGB (mMGB), and dorsal MGB (dMGB) and the six histological layers of the primary auditory cortex (AI 1-6). Therefore, a terminal deoxynucleotidyl transferase dioxyuridine triphosphate nick-end labeling assay (TUNEL) was performed in these structures 24 h, 7 days, and 14 days after noise exposure (3 h, 115 dB sound pressure level, 5-20 kHz), as well as in unexposed controls. In the dMGB, TUNEL was statistically significant elevated 24 h postexposure. AI-1 showed a decrease in TUNEL after 14 days. There was no statistically significant difference between groups for the other brain areas investigated. dMGB's widespread connection within the central auditory pathway and its nontonotopical organization might explain its prominent increase in TUNEL compared to the other MGB subdivisions and the AI. It is assumed that the onset and peak of noise-induced cell death is delayed in higher areas of the central auditory pathway and takes place between 24 h and 7 days postexposure in thalamic and cortical structures.
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Registered trials
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