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[Effect of the intense noise on hearing function and cochlea morphology in rat].

Yong Fu, Shusheng Gong, Qiuhong Xue, Guopeng Wang, Qingguo Chen

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Abstract

OBJECTIVE: To observe the changes of auditory electrophysiology and inner ear pathology in rat cochlea after the noise exposure, and to offer the experimental data for exploring the mechanism of noise-damaged cochlea. METHOD: The rats in the study group were exposed to a intense narrow band noise centered at 4 kHz at the leave of 120 dB (SPL) for 4 h. The exposed cochleae were collected at various intervals (1 or 21 days) after the noise exposure. Auditory function was monitored by measuring thresholds of auditory brain stem responses (ABR). The morphological changes in rat cochlear hair cell (HC) were examined by HC nuclei stained with Propidium iodide (PI), a fluorescent dye specifically labelling the nuclear DNA and scanning electron microscopy (SEM). The number of spiral ganglion cells was calculated using pathologic technique. RESULT: The thresholds of ABR in the study group were significantly greater than that in the normal control group (P < 0.01). Examined at 1 day after the noise exposure, normal, apoptosis, necrotic and missing out hair cell (OHC) could be distinguished with PI staining, whereas the apoptosis OHC were not found at 21 days. Significant OHC loss was found in as compared to the normal control group (P < 0.01). There was not significant difference in the calculation of spiral ganglion cells (P > 0.05). SEM revealed the injured stereocilia of OHC (disarrangement, collapse) and OHC loss in the study group, which was more severe in OHC3 than the other two rows of OHC. CONCLUSION: The intense noise used in our study could injure the rat cochlea and bring permanent threshold shift (PTS). Under this condition, the death modes of HC in the cochlea include apoptosis and necrosis in the fore part, whereas necrotic is the major mode in the evening of exposure. The injured stereocilia of OHC and OHC loss could remain the most consistent correlate of PTS.

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OBJECTIVE: To observe the changes of auditory electrophysiology and inner ear pathology in rat cochlea after the noise exposure, and to offer the experimental data for exploring the mechanism of noise-damaged cochlea. METHOD: The rats in the study group were exposed to a intense narrow band noise centered at 4 kHz at the leave of 120 dB (SPL) for 4 h. The exposed cochleae were collected at various intervals (1 or 21 days) after the noise exposure. Auditory function was monitored by measuring thresholds of auditory brain stem responses (ABR). The morphological changes in rat cochlear hair cell (HC) were examined by HC nuclei stained with Propidium iodide (PI), a fluorescent dye specifically labelling the nuclear DNA and scanning electron microscopy (SEM). The number of spiral ganglion cells was calculated using pathologic technique. RESULT: The thresholds of ABR in the study group were significantly greater than that in the normal control group (P < 0.01). Examined at 1 day after the noise exposure, normal, apoptosis, necrotic and missing out hair cell (OHC) could be distinguished with PI staining, whereas the apoptosis OHC were not found at 21 days. Significant OHC loss was found in as compared to the normal control group (P < 0.01). There was not significant difference in the calculation of spiral ganglion cells (P > 0.05). SEM revealed the injured stereocilia of OHC (disarrangement, collapse) and OHC loss in the study group, which was more severe in OHC3 than the other two rows of OHC. CONCLUSION: The intense noise used in our study could injure the rat cochlea and bring permanent threshold shift (PTS). Under this condition, the death modes of HC in the cochlea include apoptosis and necrosis in the fore part, whereas necrotic is the major mode in the evening of exposure. The injured stereocilia of OHC and OHC loss could remain the most consistent correlate of PTS.

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Available abstract

OBJECTIVE: To observe the changes of auditory electrophysiology and inner ear pathology in rat cochlea after the noise exposure, and to offer the experimental data for exploring the mechanism of noise-damaged cochlea. METHOD: The rats in the study group were exposed to a intense narrow band noise centered at 4 kHz at the leave of 120 dB (SPL) for 4 h. The exposed cochleae were collected at various intervals (1 or 21 days) after the noise exposure. Auditory function was monitored by measuring thresholds of auditory brain stem responses (ABR). The morphological changes in rat cochlear hair cell (HC) were examined by HC nuclei stained with Propidium iodide (PI), a fluorescent dye specifically labelling the nuclear DNA and scanning electron microscopy (SEM). The number of spiral ganglion cells was calculated using pathologic technique. RESULT: The thresholds of ABR in the study group were significantly greater than that in the normal control group (P < 0.01). Examined at 1 day after the noise exposure, normal, apoptosis, necrotic and missing out hair cell (OHC) could be distinguished with PI staining, whereas the apoptosis OHC were not found at 21 days. Significant OHC loss was found in as compared to the normal control group (P < 0.01). There was not significant difference in the calculation of spiral ganglion cells (P > 0.05). SEM revealed the injured stereocilia of OHC (disarrangement, collapse) and OHC loss in the study group, which was more severe in OHC3 than the other two rows of OHC. CONCLUSION: The intense noise used in our study could injure the rat cochlea and bring permanent threshold shift (PTS). Under this condition, the death modes of HC in the cochlea include apoptosis and necrosis in the fore part, whereas necrotic is the major mode in the evening of exposure. The injured stereocilia of OHC and OHC loss could remain the most consistent correlate of PTS.

Key concepts: Spiral ganglion, Cochlea, Stereocilia (inner ear), Hair cell, Propidium iodide, Noise-induced hearing loss, Anatomy, Noise exposure

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