Abstract
Noise-induced hearing loss (NIHL) relates closely to auditory cortex (AC) injury, so countermeasures aiming at the AC recovery would be of benefit. In this work, the effect of hyperbaric oxygen treatment on NIHL was elucidated, which was imposed on mice before (HBOP), during (HBOD) or after (HBOA) noise exposure. Morphology of neurons was assayed by hematoxylin-eosin or Nissl staining. Ceramide (Cer) level was measured through immunohistochemistry analysis. Apoptotic neurons were counted using transferase-mediated dUTP nick end labeling (TUNEL) staining. We demonstrated that the intense, broad band noise raised the threshold of auditory brainstem response, evoked neuronal degeneration or apoptosis and triggered the Cer accumulation in AC, all of which were restored significantly by HBOP, but not HBOD or HBOA. Cer over-generation reversed the advantages of HBOP significantly, while its curtailment recapitulated the effect. Next, noise exposure raised the superoxide or malondialdehyde (MDA) production which was blocked by HBOP or Cer repression. Oxidative control not only attenuated the hearing loss or neurodegeneration but, in turn, reduced the Cer formation significantly. In summary, mutual regulation between Cer and oxidative stress underlies the HBOP’s curative effect on hearing loss and neuronal damage in noise-exposed mice.
Highlights
Noise exposure has relation to complex manifestations such as hearing loss, tinnitus, reduced speech intelligibility and hyperacusis, which is largely ascribed to the neuronal damage in the central auditory pathway [1]
We examined the improvement of auditory sensitivity and neuronal morphology in auditory cortex (AC) of mice with the Hyperbaric oxygen therapy (HBOT) exerted before, during, or after noise exposure
To verify the effect of HBOT on hearing loss and neurodegeneration, Auditory Brainstem Response (ABR) threshold and neuronal morphology were examined in control and noise-exposed mice
Summary
Noise exposure has relation to complex manifestations such as hearing loss, tinnitus, reduced speech intelligibility and hyperacusis, which is largely ascribed to the neuronal damage in the central auditory pathway [1]. Multiple labs have revealed the massive loss of cell density and apoptosis of neurons in higher auditory structures like medial geniculate body (MGB) and primary auditory cortex (A1) in the wake of intense noise exposure [1,2,3,4,5]. In this respect, keeping the auditory neurons from noise elicited damage stands out crucial for the improvement of the hearing performance. The action of HBOT on noise-induced hearing loss and auditory neuronal damage is still under debate
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