Hearing loss impairs perceptual and neural processing at fast time scales

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PROJECT SUMMARY Developmental hearing loss (HL) can impair the perception of amplitude modulations (AM), which are the temporal fluctuations of sound level that support speech comprehension, rhythm, prosody, and pitch. In fact, temporal processing for fast AM rates seems to be most vulnerable to HL. One explanation for these perceptual deficits is that developmental HL degrades the neural representation of AM within the auditory system. Thus, this proposal will evaluate HL-related neural and behavioral deficits in fast temporal processing through a systems-level approach. Envelope following responses (EFRs), which reflect peripheral and subcortical generators, will be recorded from normal hearing (NH) and HL-reared gerbils to assess brainstem temporal processing. Extracellular responses will then be obtained telemetrically from core auditory cortex (ACx) neurons as gerbils perform an auditory psychophysical task that assesses AM sensitivity or rate discriminability. The core hypothesis is that developmental conductive HL disrupts cortical AM response magnitude and tuning, especially at fast modulation rates, thereby degrading perceptual sensitivity and temporal resolution, respectively. I will explore this hypothesis with three aims. Specific Aim 1 will determine whether developmental HL leads to deficits in AM detection. Gerbils will be trained on an AM detection task that spans a broad range of AM rates and then subsequently tested across a range of AM depths for a single AM rate. Psychometric performance will be compared between NH and HL groups to evaluate the degree of HL-related deficits. Specific Aim 2 will determine whether developmental HL leads to deficits in AM rate discrimination. The task structure is identical to the AM detection task, with the exception that gerbils are required to discriminate between separate AM rates. Specific Aim 3 will determine whether degraded brainstem or cortical encoding mechanisms could account for developmental HL-related deficits in AM sensitivity (Aim 1) and rate discriminability (Aim 2). First, EFRs will be obtained across AM rates in all gerbils before ACx electrode implantation, and then again after all awake-behaving sessions have been acquired. Gerbils will then be implanted with an electrode array in the left core ACx and cortical responses will be recorded wirelessly during task performance and separate sessions when the gerbils are disengaged from the task. Neural sensitivity across brainstem and cortical levels will be compared within and between NH and HL groups. Together, these aims will further the understanding of the neural mechanisms, and their origins, underlying HL-related deficits that involve encoding envelope cues associated in communication and other perceptual qualities in speech. The long-term implication of this work is that specific HL-related impairments in speech and language processing can be attributed to peripheral or central nervous system deficits, which can be targeted for therapeutic intervention and restoration.