The changes of phosphorylated c-Jun expression in spiral ganglion after exposed to noise.
- Author:
Yin XIA
1
;
Haishan LONG
;
Demin HAN
;
Shusheng GONG
;
Li LEI
;
Jinfeng SHI
;
Erzhong FAN
;
Ying LI
;
Qing ZHAO
Author Information
1. Department of Otolaryngology Head and Neck Surgery, Beijing Tongren Hospital, Capital Medical University, Key Laboratory of Otolaryngology Head and Neck Surgery, Ministry of Education, Beijing, 100730, China.
- Publication Type:Journal Article
- MeSH:
Acoustic Stimulation;
Animals;
Auditory Threshold;
Cochlea;
metabolism;
Hearing Loss, Noise-Induced;
metabolism;
JNK Mitogen-Activated Protein Kinases;
metabolism;
Mice;
Mice, Inbred Strains;
Spiral Ganglion;
metabolism
- From:
Journal of Clinical Otorhinolaryngology Head and Neck Surgery
2009;23(4):174-177
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To investigate the mechanism of hearing pathway NMDAR regulating the changes of phosphorylated c-Jun expression in spiral ganglion after exposed Kunming mice to neural injury noise stimulation to induce permanent or temporary threshold shift.
METHOD:To compare the different expressions of the key components (phosphorylated C-Jun) of NMDAR signal pathway during neural injury stimulation by Immunohistochemistry in CG.
RESULT:The levels of phosphorylated c-Jun remarkably, increased in the spiral ganglion after 8 h, 48 h, 7 d and 14 d following noise trauma induced permanent threshold shift (PTS), and the numbers of positive cells reduced gradually. The similar changes occur in mice treated with MK-801 30 minutes before and after 3 h trauma induced PTS. After 48 h of noise induced TTS, the expression of Phosphorylated c-Jun return the level of normal control.
CONCLUSION:The expressions of phosphorylated c-Jun are time-related and uniform in the time and position in CG after noise trauma. MK-801 can alleviate the damage of noise trauma by altered the NMDA receptor-mediated calcium influx. Therefore, the NMDA receptors may involved in the damage of inner ear in common.
