4.4 Article

Up-regulation of Nob1 in the rat auditory system with noise-induced hearing loss

Journal

NEUROSCIENCE LETTERS
Volume 491, Issue 1, Pages 79-82

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2011.01.010

Keywords

Nob1; Noise induced hearing loss; Cochlea

Categories

Funding

  1. National Natural Scientific Foundation of China [30872857, 30871141, 30930098, 30772261]

Ask authors/readers for more resources

The Nob1 gene is assumed to be associated with transcription regulation and may play important roles in mediating some physiological and pathological functions. Here, the rats were randomized equally into experimental group and control group. In experimental group, all subjects were exposed to 4-kHz octave-band noise at 110 dB SPL, 8 h per day for 7 days consecutively. Auditory thresholds were assessed by auditory brainstem response, prior to and 1 h after the cessation of noise exposure. Then, we investigated for the first time the expression of Nob1 in noise-exposed and noise-unexposed rats by quantitative polymerase chain reaction. The distribution of Nob1 in rat cochlea was further examined by immunohistochemistry. The results indicated that the hearing threshold was significantly higher in the noise-injured group than in the uninjured group after noise exposure. Nob1 mRNA was present at higher levels in regions of the noise-injured cochlea. As for noise-exposed rats, Nob1 expression was positive in the inner and outer hair cells of the organ of Corti and spiral ganglion neurons, but it undetectable in the uninjured cochlea. Therefore. Nob1 may play an important role in auditory function following acoustic trauma and can be used as a new target for the treatment of noise-induced hearing loss. (c) 2011 Elsevier Ireland Ltd. All rights reserved.

Authors

I am an author on this paper
Click your name to claim this paper and add it to your profile.

Reviews

Primary Rating

4.4
Not enough ratings

Secondary Ratings

Novelty
-
Significance
-
Scientific rigor
-
Rate this paper

Recommended

No Data Available
No Data Available