Can long-term exposure to non-damaging noise lead to hyperacusis or tinnitus?
Abstract
Hearing loss triggers changes in the central auditory system, some maladaptive. A region of primary auditory cortex (A1) deprived of input responds more strongly to cochlear lesion-edge frequencies, and its spontaneous firing rate (SFR) increases. This spontaneous and sound-evoked hyperactivity has been associated with tinnitus and hyperacusis, respectively. Regional increases in A1 spontaneous and sound-evoked activity are also observed after long-term exposure to non-damaging levels of noise. Adult cats exposed to such noise bands had suppressed SFR and evoked activity in the A1 region mapped to the noise band, but had increased SFR and evoked activity in A1 regions above and below the band. We hypothesized that, post-exposure, frequencies within the noise band should for some time be perceived as softer than before (hypoacusis), whereas frequencies outside of the noise band might be perceived as louder than before (hyperacusis), and might even be internalized as tinnitus. To investigate this possibility, adult CBA/Ca mice were exposed for >2 months to 8–16 kHz bandpass noise at 70 dB SPL, and tested for hypo/hyperacusis and tinnitus using prepulse inhibition (PPI) of the acoustic startle reflex (ASR), and gap-PPI of the ASR (GPIAS), respectively. ABRs and DPOAEs showed that the 70 dB SPL exposure was indeed non-damaging, whereas the same noise band at 75 dB SPL appeared to cause cochlear synaptopathy. Contrary to hypothesis, long-term exposure to non-damaging noise had no significant effect on PPI ASR and GPIAS testing. These negative findings nevertheless have important implications for PPI and GPIAS testing, and for the mechanisms of tinnitus and hyperacusis.
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