Cell-cell junctions: a target of acoustic overstimulation in the sensory epithelium of the cochlea

BMC Neuroscience

Bo Hua Hu¹  Guiliang Zheng² 

[1] Center for Hearing and Deafness, State University of New York at Buffalo, Buffalo, USA;Present affiliation: Department of Otorhinolaryngology Head and Neck Surgery, Changhai Hospital, Second Military Medical University, Shanghai, China

关键词: Permeability;    Dextrans, organ of Corti;    Hair cells;    Basilar membrane;    Cochlea;    Cell junctions;    Acoustic overstimulation;   

Others  :  1170660
DOI  :  10.1186/1471-2202-13-71

 received in 2012-03-23, accepted in 2012-06-19,  发布年份 2012

【 摘 要 】

Background

Exposure to intense noise causes the excessive movement of the organ of Corti, stretching the organ and compromising sensory cell functions. We recently revealed changes in the transcriptional expression of multiple adhesion-related genes during the acute phases of cochlear damage, suggesting that the disruption of cell-cell junctions is an early event in the process of cochlear pathogenesis. However, the functional state of cell junctions in the sensory epithelium is not clear. Here, we employed graded dextran-FITC, a macromolecule tracer that is impermeable to the organ of Corti under physiological conditions, to evaluate the barrier function of cell junctions in normal and noise-traumatized cochlear sensory epithelia.

Results

Exposure to an impulse noise of 155 dB (peak sound pressure level) caused a site-specific disruption in the intercellular junctions within the sensory epithelium of the chinchilla cochlea. The most vulnerable sites were the junctions among the Hensen cells and between the Hensen and Deiters cells within the outer zone of the sensory epithelium. The junction clefts that formed in the reticular lamina were permeable to 40 and 500 but not 2,000 kDa dextran-FITC macromolecules. Moreover, this study showed that the interruption of junction integrity occurred in the reticular lamina and also in the basilar membrane, a site that had been considered to be resistant to acoustic injury. Finally, our study revealed a general spatial correlation between the site of sensory cell damage and the site of junction disruption. However, the two events lacked a strict one-to-one correlation, suggesting that the disruption of cell-cell junctions is a contributing, but not the sole, factor for initiating acute sensory cell death.

Conclusions

Impulse noise causes the functional disruption of intercellular junctions in the sensory epithelium of the chinchilla cochlea. This disruption occurs at an early phase of cochlear damage. Understanding the role of this disruption in cochlear pathogenesis will require future study.

【 授权许可】

   
2012 Zheng and Hu. licensee BioMed Central Ltd.

【 图 表 】

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