Abstract # 7875 Event # 128:

Scheduled for Saturday, August 26, 2017 04:15 PM-04:30 PM: (Grand Ballroom) Oral Presentation


M. Valero1, S. Hauser2, J. Burton2, G. Recanzone3, T. Hackett2, R. Ramachandran2 and M. Liberman1
1Massachusetts Eye and Ear Infirmary/Harvard Medical School, 243 Charles St , Boston, MA 02129, USA, 2Vanderbilt University School of Medicine, 3University of California, Davis
     The audiogram has long been regarded as the gold-standard test of hearing ability. However, recent rodent research has demonstrated that noise exposures causing only temporary threshold shifts can induce a permanent loss of ~50% of synapses on inner hair cells (IHCs) that is undetectable by audiograms. This is because the ‘cochlear amplifier’ (outer hair cells; OHCs) and the low-threshold auditory nerve fibers (ANFs) are spared. Synaptopathy is selective for the normally high-threshold ANFs that are crucial for signal-detection in noise. This likely degrades speech-in-noise performance despite normal audiograms, is referred to as ‘hidden hearing loss.’ When OHCs are also damaged, both threshold and suprathreshold performance are compromised. To assess the generality of these findings to primates, we compared the normal cochlear innervation of young, unexposed macaques to that of noise-overexposed or aging animals. Cochlear function was assayed for 8-wks. Following 108-dB SPL noise, monkeys with normal audiograms had 15-30% synaptopathy. Following 146-dB SPL noise, 50-80% synaptopathy was accompanied by widespread OHC loss, threshold shifts, and suprathreshold deficits. Aging, unexposed monkeys had varying degrees of synaptopathy with little HC loss. These data indicate that primates are susceptible to noise-induced and age-related synaptopathy. In the future, we will use macaques as a model for developing diagnostics and testing emerging therapies for cochlear synaptopathy.