Lateral wall histopathology and endocochlear potential in the noise-damaged mouse cochlea

• Published in: Journal of the Association for Research in Otolaryngology 2003-09, Vol.4 (3), p.339-352
• Main Authors: Hirose, Keiko, Liberman, M Charles
• Format: Article
• Language: English
• Subjects: Animals; Auditory Threshold; Cochlea - pathology; Cochlea - physiopathology; Cochlea - ultrastructure; Hearing Loss, Noise-Induced - pathology; Male; Mice; Mice, Inbred CBA; Microscopy, Electron; Noise - adverse effects; Spiral Ganglion - pathology
• ISSN: 1525-3961; 1438-7573
• DOI: 10.1007/s10162-002-3036-4

Noise exposure damages the stria and spiral ligament and may contribute to noise-induced threshold shift by altering the endocochlear potential (EP). The aim of this study was to correlate lateral wall histopathology with changes in EP and ABR thresholds. CBA/CaJ mice were exposed to octave band (8-16 kHz) noise for 2 h at intensities ranging from 94 to 116 dB SPL and evaluated 0 h to 8 weeks postexposure. EP in control mice averaged 86 and 101 mV in apical and basal turns, respectively. The 94 dB exposures caused a 40 dB temporary threshold shift (TTS), and there was with no corresponding change in EP. The 112 and 116 dB exposures caused >60 dB threshold shifts at 24 h, and EP was transiently decreased, e.g., to 21 and 27 mV in apical and basal turns after 116 dB. By 1 week postexposure, EP returned to control values in all exposure groups, although those exposed to 112 or 116 dB showed large permanent threshold shifts (PTS). Cochleas were plastic-embedded and serial-sectioned for light microscopic and ultrastructural analysis. Acute changes included degeneration of type II fibrocytes of the spiral ligament and strial edema. The strial swelling peaked at 24 h when significant EP recovery, had taken place, suggesting that these changes reflect compensatory volume changes. In the chronic state, massive loss of type II fibrocytes and degeneration of strial intermediate and marginal cells was observed with drastic reduction in membrane surface area. The results suggest that EP shifts do not occur with TTS and also do not add significantly to PTS in the steady state. However, EP loss could contribute to acute threshold shifts that resolve to a PTS. EP recovery despite significant strial degeneration may be partly due to decreased transduction current caused by hair cell damage.