Acoustic trauma-induced auditory cortex enhancement and tinnitus

There is growing evidence suggests that noise-induced cochlear damage may lead to hyperexcitability in the central auditory system (CAS) which may give rise to tinnitus. However, the correlation between the onset of the neurophysiological changes in the CAS and the onset of tinnitus has not been well studied. To investigate this relationship, chronic electrodes were implanted into the auditory cortex (AC) and sound evoked activities were measured from awake rats before and after noise exposure. The auditory brainstem response (ABR) was used to assess the degree of noise-induced hearing loss. Tinnitus was evaluated by measuring gap-induced prepulse inhibition (gap-PPI). Rats were exposed monaurally to a high-intensity narrowband noise centered at 12 kHz at a level of 120 dB SPL for 1 h. After the noise exposure, all the rats developed either permanent (>2 weeks) or temporary (<3 days) hearing loss in the exposed ear(s). The AC amplitudes increased significantly 4 h after the noise exposure. Most of the exposed rats also showed decreased gap-PPI. The post-exposure AC enhancement showed a positive correlation with the amount of hearing loss. The onset of tinnitus-like behavior was happened after the onset of AC enhancement.