Abstract
Age-related hearing loss is a ubiquitous malady in the geriatric population, yet the underlying neural mechanisms remain incompletely understood. We compared onset and offset responses of single neurons in the primary (A1), rostral (R), and caudolateral (CL) areas of the auditory cortex using spectral, spatial, and temporal stimuli in a young macaque monkey with normal-hearing and an aged macaque monkey with high frequency hearing loss. In the young monkey, core areas exhibited a significantly higher proportion of neurons responsive to both the onset and the offset of stimuli compared to the belt area CL, indicating functional differentiation. However, this distinction diminished with age, with the proportion of neurons with both onset and offset responses becoming more uniform across cortical areas. Onset firing rates were generally higher in the aged monkey, but with a lower signal-to-noise ratio, suggesting increased neural excitability but reduced response fidelity. Notably, CL neurons in the aged monkey exhibited a significantly greater disparity between the best frequencies for onset and offset responses, suggesting reduced spectral precision. Additionally, spectral tuning bandwidths (BW) were broader in the CL neurons in the aged monkey, while in the young monkey, A1 neurons exhibited significantly narrower onset BWs compared to offset BWs, a distinction that was lost in the aged monkey. These findings highlight a fundamental asymmetry in auditory cortical processing and suggest that belt area CL is particularly susceptible to age-related changes. Understanding these neural mechanisms provides insights into auditory aging and potential strategies for mitigating hearing deficits. NEW AND NOTEWORTHY: This study finds that there are significant differences in the temporal fidelity of auditory cortical neuronal responses as a function of natural aging, particularly in the belt cortical field CL compared to core areas A1 and R. These differences are stimulus dependent and are consistent with known auditory processing deficits in geriatric human subjects.