The Ascending Auditory Pathway In The Brain Stem Of The Monkey PDF Download

Age-related hearing loss is a complex auditory disorder that is associated with a gradual decline of auditory perceptions. Sound localization is one of many auditory perceptions that get impaired in the aged. While sound localization has been studied in great detail at the behavioral level in a variety of young and middle aged animals, little is known about how the neuronal processing breaks down in the aged to impair our perception acoustic space. The current set of studies presented in the forthcoming chapters is part of a series of experiments to develop a primate model of age-related hearing loss that are designed to further our understanding of both the structural and functional changes that accompany aging. In the present series of experiments, several anatomical and electrophysiological studies were designed to characterize and correlate age-related hearing loss in the rhesus macaque monkey (Macaca mulatta) to determine if the auditory system compensates for a reduction in drive from the periphery. A requisite was first to determine if rhesus monkeys experience age-related hearing loss. This was accomplished by linking changes in hearing level to distinct histopathologies in the cochlea. Age-related hearing loss was assessed by the auditory brainstem response (ABR) to clicks and pure tones across a population of rhesus macaque monkeys at the California National Primate Research Center at the University of California of Davis. Histological specimens were then randomly collected and examined for distinct histopathological changes in the cochlea. Multiple regression was used to tease apart the contributions of the observed histopathologies on ABR thresholds. Consistent with findings in humans, rhesus monkeys were found to experience progressive age-related hearing loss with a concomitant increase in the number of histopathologies in the cochlea. We found that spiral ganglion cell loss and outer hair cells loss made significant contributions to ABR threshold increases across the spectrum. At the level of the midbrain, the density of parvalbumin neurons in the inferior colliculus was found to increase with age. Interestingly, there was no direct relationship between the densities of parvalbumin cells in the inferior colliculus with the hearing ability of the monkeys. One explanation for this result is that the increase in the density of parvalbumin neurons produced a functional advantage in the processing of simple stimuli. Lastly, we collected and examined neuronal responses in A1 and CL of young and aged rhesus monkeys to investigate the role of age-related hearing loss on auditory cortical responses to spatial stimuli in azimuth. Interestingly, we found a differential increase in driven firing rates and a decrease in the efficacy of inhibition across defined periods of the neuronal response that contributed to broader spatial tuning properties in both A1 and CL of aged rhesus monkeys. These results suggest that spatial tuning may reflect a maladaptive compensatory mechanism within the central auditory system that overcompensation for changes in the periphery. Overall, the combined results of these studies suggest that the decline of auditory perceptions associated with age-related hearing loss maybe generated by the central nervous systems own mechanisms to adapt to changes in peripheral drive. It is proposed that this process is a major contributor to age-related cognitive decline.