Every day, we are bombarded with noise. Trucks rumbling, music blasting, horns honking, crowds talking -- we live in a loud world. Sometimes, when we are exposed to a particularly intense noise, we seem to perceive sound differently afterwards.

“You know the feeling, if you have been to a loud rock concert?” asked Tommi Anttonen, a postdoctoral researcher at the University of Southern Denmark and Kavli-Grass Fellow at the Marine Biological Laboratory (MBL). “You kind of feel like, for a while, you can’t hear well after that.” This phenomenon is sometimes called temporary hearing loss, and Anttonen is fascinated by it. 

How this hearing loss happens on a biological level is something of a mystery. It could happen in the inner ear, the auditory nerve, the brain itself, or some combination therein. Anttonen is studying this phenomenon using a model organism whose inner ears are quite similar to our own, a small bird called a zebra finch. He wants to understand what happens deep inside birds’ inner ears when they experience temporary hearing loss. In doing so, he hopes to help lay the foundation for medical therapies for people suffering from hearing loss.

Tommi Anttonen adjusting the microscope he uses to study hair cell vesicles in zebra finch inner ears. Credit: William von Herff
Tommi Anttonen in the Grass Lab at MBL, adjusting the microscope he uses to study hair cell vesicles in zebra finches. Credit: William von Herff

The Mechanics of Hearing Loss

Hearing is our brain’s way of processing vibrations in the air. When these vibrations travel into the ear, through the eardrum and reach your inner ear, they hit extremely sensitive cells called hair cells. This force causes the hair cells to jiggle, which activates tiny capsules, called vesicles, containing the neurotransmitter glutamate. These vesicles fuse with the hair cell membrane, releasing the glutamate outside the hair cell. These neurotransmitters stimulate glutamate-sensitive cells in the auditory nerve, relaying a signal to the brain that we interpret as sound. 

When hair cells are slightly overstimulated, however, we get temporary hearing loss. Anttonen hypothesizes that overstimulation causes the hair cells to “tire out”, so they release fewer neurotransmitter vesicles. This, he thinks, is partly why we struggle to hear well after being exposed to loud sound: fewer glutamate-filled vesicles means a weaker signal is relayed to the brain.

Each zebra finch in Anttonen’s study will first have its hearing tested. Anttonen will attach electrodes to the birds’ heads to measure auditory brainstem activity in response to sound, similar to a hearing screening in a newborn. Then, the birds will be exposed to a noise for just long enough to temporarily stress their inner ears. Anttonen will then compare the birds’ auditory brainstem responses after the noise exposure to assess exactly how it impacted their hearing.

The second half of the experiment involves measuring how many neurotransmitter vesicles are released before and after temporary hearing loss. If fewer vesicles are released from the hair cells of hearing-damaged birds, it would support Anttonen’s theory that vesicle release plays a role in temporary hearing loss.

Anttonen will also examine the finches’ inner ears for something very unusual: fused hair cells. When he was working with mice, Anttonen and his colleagues found that some damaged hair cells seem to link to each other, possibly to share resources. In doing so, they may limit the ear’s precision: The two fused hair cells, which would typically respond in slightly different ways to sound, act as one. Repeat this across multiple hair cells, and the inner ear may become less sensitive over time. 

Both of these phenomena -- restricted vesicle release and fused hair cells -- may contribute to temporary hearing loss in these birds. Anttonen stresses that “understanding those mechanisms would maybe give us some opportunities to help people with hearing loss.” Currently, reversing hearing loss in humans is extremely difficult. “If we could understand the cellular mechanisms of noise damage,” Anttonen said, “maybe we could find pharmacological ways of protecting the inner ear.”

Besides, he said, “How fun would it be to have a ‘disco pill’ that you will take before you go to the disco and your hearing won’t go away?”