Abstract
BackgroundExposure 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.ResultsExposure 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.ConclusionsImpulse 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.
Highlights
Exposure to intense noise causes the excessive movement of the organ of Corti, stretching the organ and compromising sensory cell functions
We found that the lesions in the hair cells were located in the sensory epithelium between the upper first and the lower second cochlear turns (Figure 1C), which in the chinchilla cochlea corresponds to a frequency range of 2–4 kHz [29]
The current investigation documents the dysfunction of cell-cell junctions in the cochlear sensory epithelium following exposure to a high level of impulse noise
Summary
Exposure to intense noise causes the excessive movement of the organ of Corti, stretching the organ and compromising sensory cell functions. Cell-cell junctions are specialized regions of contact between the apposed plasma membranes of neighboring cells and are responsible for the maintenance of tissue architecture, cell communication, mechanical links between cells, and tissue homeostasis [1,2] Based on their morphology, cell-cell junctions in the mammalian organ of Corti have been divided into tight, gap, adherens, and desmosome junctions [3,4,5,6]. Mice with a conditional deficiency in the expression of vezatin, a ubiquitous adherens junction protein, exhibit an increased susceptibility to acoustic trauma [17] This finding suggests that vezatin participates in the regulation of cochlear responses to acoustic injury. These observations imply a role for the molecular response of cell-cell junctions in cochlear pathogenesis following acoustic trauma
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