# Behavioral and physiological consequences of auditory nerve loss

> **NIH NIH R01** · UNIVERSITY OF ROCHESTER · 2022 · $327,250

## Abstract

Permanent loss of auditory-nerve (AN) spiral ganglion neurons is a prevalent cochlear pathology in humans
that does not impact clinical audiometric thresholds in quiet. Reduced sensory input to the auditory pathway
could potentially degrade speech-perception abilities in affected individuals, but support for this hypothesis is
unclear. The goal of the proposed study is to pinpoint aspects of auditory perception impacted by AN damage
and characterize the physiological changes underlying perceptual impairment. Many natural signals, including
speech, contain complex patterns of amplitude modulation (hereafter, ‘modulation’) that are processed by
modulation-tuned neurons in the central nervous system. Modulation tuning emerges in the midbrain due to
inhibition, and can play a key processing role in noise by segregating competing sounds into discrete
processing streams based on differences in modulation frequency. Building upon prior findings of diminished
inhibitory signaling following AN injury, the proposed research will test the hypothesis that AN damage
selectively impairs complex-signal perception in noise while sparing audiometric thresholds due to a deficit in
neural modulation tuning. Behavioral and neurophysiological studies will be conducted in the budgerigar, an
avian model species capable of mimicking speech. Strengths of the budgerigar model system include human-
like behavioral performance on complex-listening tasks and midbrain processing mechanisms shared with
mammals, including many neurons with prominent modulation tuning. Furthermore, selective AN damage can
be induced in budgerigars using the glutamate analog kainic acid. New behavioral and neurophysiological
experiments will investigate the impact of kainic-acid induced AN damage on auditory processing. Aim 1 will
use operant-conditioning procedures in behaviorally trained animals to identify aspects of auditory perception
impacted by AN damage. Preliminary data support our hypothesis that AN damage has no effect on
audiometric thresholds in quiet yet can impair performance of tasks that rely on modulation tuning. Aim 2 will
use extracellular midbrain recordings in awake animals to quantify effects of AN damage on neural inhibition,
modulation tuning, and encoding of complex speech-like signals in competing noise. We hypothesize that AN
damage will reduce the strength of modulation tuning due to diminished inhibition, and consequently degrade
encoding of synthetic vowels and consonants in noise. Aim 3 will use single-fiber AN recordings to test the
hypothesis that AN response properties in budgerigars are similar to those found in mammals and other avian
species, with higher-threshold fibers lost following kainic-acid exposure. New physiological results will be used
to refine a computational model of subcortical auditory processing. Completion of these aims will provide
crucial insight into the impact of AN damage on auditory perception of simple and complex sounds and the
change...

## Key facts

- **NIH application ID:** 10434851
- **Project number:** 5R01DC017519-04
- **Recipient organization:** UNIVERSITY OF ROCHESTER
- **Principal Investigator:** Kenneth Stuart Henry
- **Activity code:** R01 (R01, R21, SBIR, etc.)
- **Funding institute:** NIH
- **Fiscal year:** 2022
- **Award amount:** $327,250
- **Award type:** 5
- **Project period:** 2019-07-01 → 2024-06-30

## Primary source

NIH RePORTER: https://reporter.nih.gov/project-details/10434851

## Citation

> US National Institutes of Health, RePORTER application 10434851, Behavioral and physiological consequences of auditory nerve loss (5R01DC017519-04). Retrieved via AI Analytics 2026-05-23 from https://api.ai-analytics.org/grant/nih/10434851. Licensed CC0.

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