Time course of cell death due to acoustic overstimulation in the mouse medial geniculate body and primary auditory cortex

Autor: Moritz Gröschel, Ira Strübing, Arne Ernst, Dietmar Basta, Felix Fröhlich
Rok vydání: 2017
Předmět:
0301 basic medicine
Inferior colliculus
Programmed cell death
Pathology
medicine.medical_specialty
Time Factors
Apoptosis
Biology
Auditory cortex
Cochlear nucleus
lcsh:RC963-969
03 medical and health sciences
Speech and Hearing
Mice
0302 clinical medicine
Central hearing loss
medicine
In Situ Nick-End Labeling
Animals
Hearing Loss
Central
Auditory Cortex
TUNEL assay
Cell Death
Public Health
Environmental and Occupational Health
Geniculate Bodies
noise-induced apoptosis
Anatomy
Medial geniculate body
lcsh:Otorhinolaryngology
lcsh:RF1-547
noise-induced hearing loss
TUNEL-staining
030104 developmental biology
Otorhinolaryngology
Terminal deoxynucleotidyl transferase
Acoustic Stimulation
Hearing Loss
Noise-Induced
lcsh:Industrial medicine. Industrial hygiene
Female
Original Article
Noise
030217 neurology & neurosurgery
Zdroj: Noise & Health
Noise and Health, Vol 19, Iss 88, Pp 133-139 (2017)
ISSN: 1463-1741
Popis: 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.
Databáze: OpenAIRE
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