University of Pittsburgh
Active corticofugal control of sound localization in noise
Locating sounds in a noisy environment is essential for everyday communication, and it is a task we accomplish with our bodies as much as with our ears. Listeners naturally turn their heads and orient toward a sound source, and these movements change the signal arriving at each ear from moment to moment, giving the brain additional information about where the sound originated. Exposure to loud noise permanently damages the connections between the inner ear and the auditory nerve, degrading the fine detail required to separate competing sound sources. The result is that many people report considerable difficulty following a conversation in a crowded room despite a normal audiogram, a core complaint in central auditory processing disorder. Almost everything known about how the brain computes sound location, however, comes from experiments in which the head is held still, eliminating the very movements listeners rely on in natural settings.
This project asks how noise-induced hearing loss disrupts active listening, and which neural circuit is responsible. We have developed a task in which mice move freely around an arena surrounded by speakers, searching for a target sound while a competing distractor sound plays simultaneously. Video tracking allows us to measure the strategies they use: pausing to scan the head from side to side, correcting an initial trajectory with a sharp turn, or spiraling gradually toward the target. Comparing these strategies before and after noise exposure will reveal whether noise damage degrades not only what an animal hears, but how it searches. We will then examine the descending pathway connecting auditory cortex, which identifies the features of a sound, to the superior colliculus, a midbrain structure containing a map of space that issues commands to orient the head and body. We hypothesize that this pathway converts sound features into a direction to turn, and that noise damage dysregulates it. We will record from the pathway during behavior, suppress it in normal-hearing mice to determine whether this reproduces the deficit, and activate it in noise-exposed mice to determine whether the deficit can be reversed.