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Modified Experimental Conditions for Noise-Induced Hearing Loss in Mice and Assessment of Hearing Function and Outer Hair Cell Damage
Published on: February 10, 2023
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Acoustic overstimulation activates 5'-AMP-activated protein kinase through a temporary decrease in ATP level in the
Reiko Nagashima1, Taro Yamaguchi, Nobuyuki Kuramoto
1Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University, Hirakata, Osaka 573-0101, Japan.
Neurochemistry International
|September 13, 2011
Summary
Mitochondrial dysfunction causes inner ear disorders. This study shows that noise-induced hearing loss activates 5'-AMP-activated protein kinase (AMPK) and JNK in the cochlea due to ATP depletion.
Area of Science:
- Oto-neurology
- Cellular biology
- Biochemistry
Background:
- Inner ear disorders are linked to mitochondrial dysfunction and reduced ATP levels.
- 5 AMP-activated protein kinase (AMPK) is activated by metabolic stress and increased AMP/ATP ratio.
Purpose of the Study:
- To investigate the role of AMPK-derived signals in noise-induced hearing loss.
- To determine if acoustic overstimulation activates AMPK in the mouse cochlea.
Main Methods:
- Mice were exposed to varying sound pressure levels (SPL) of octave band noise.
- Levels of phospho-AMPKα (p-AMPKα), phospho-c-Jun N-terminal kinase (p-JNK), and ATP were measured in cochlear structures.
Main Results:
- Noise exposure at 110 or 120 dB SPL caused outer hair cell death and permanent hearing loss.
- Acoustic overstimulation elevated p-AMPKα and p-JNK levels in the cochlear lateral wall structures.
- ATP levels temporarily decreased in the spiral ligament, correlating with noise intensity.
Conclusions:
- AMPK and JNK activation in the cochlear spiral ligament are linked to ATP depletion.
- These molecular events precede permanent hearing loss from acoustic overstimulation.
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