Persistent auditory-nerve deficits and shifted spontaneous-rate composition following noise-induced temporary threshold shift in chinchillas

Listeners with clinically normal audiograms can still experience difficulty hearing in noise, a problem often discussed in the context of "hidden hearing loss". Cochlear synaptopathy has been proposed as one potential mechanism underlying these deficits, but reliable physiological assays for detecting synaptopathy remain challenging. The present study examined the effects of noise exposure that produced temporary threshold shift (TTS) in chinchillas using cochlear histology, noninvasive physiological measures, and single-unit auditory-nerve recordings. Histology confirmed persistent loss of inner-hair-cell synapses following exposure. ABR thresholds recovered and DPOAE levels were preserved 2 weeks after exposure, and many auditory-nerve response properties, including tuning and rate-level response metrics, showed no significant post-exposure differences among surviving fibers. However, several suprathreshold and timing-related abnormalities persisted after exposure. Suprathreshold ABR measures showed reduced Peak 1 amplitudes and prolonged Peak 5-Peak 1 latencies, while single-unit recordings revealed a reduced proportion of low-SR fibers in the exposed population. Selective post-exposure differences were also observed in auditory-nerve timing and modulation-related metrics, including reduced first-spike timing variability, increased adapted firing rate, reduced envelope-coding strength, and prolonged envelope-coding delay, suggesting residual disruption of suprathreshold temporal coding that may be perceptually relevant for listening in noise. These findings suggest that recovered TTS produces subtle but persistent neural changes that are not fully captured by conventional threshold-based measures. The results may help explain why diagnosis of cochlear synaptopathy remains challenging, and support the use of suprathreshold, latency-sensitive, and modulation-based physiological assays to detect residual neural effects of cochlear synaptopathy.