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If some speakers in your sound system were broken, you might try to compensate by cranking up the volume on the ones that still work. It turns out that the brain does the same thing when damaged hair cells in the ear lead to hearing loss – and this could be causing your tinnitus.
Sensory hair cells are tiny structures in the cochlea that wave like blades of grass in the wind – but in this case, it’s the pressure of sound waves that gets them moving. When they do, they create electrical signals that are funneled through nerve fibers to the brain, to process what you’re hearing.
But a small percentage of these nerves actually run in the opposite direction, from the brain to the cochlea. Scientists have long been puzzled by the function of these backwards channels, and it’s hard to study their activity while people or animals are awake.
In the new study, scientists at the University of Southern California (USC) used an intriguing imaging tool to see what’s going on in there. The technique is called optical coherence tomography (OCT), which involves creating a 3D image of tissue using light waves. It’s currently used to scan the retina to diagnose conditions like glaucoma, but the team adapted it for use in the ear.
“OCT lets us look down the ear canal, through the eardrum and bone into the cochlea, and measure how it’s working – non-invasively and without pain,” said John Oghalai, lead author of the study. “What’s exciting about this is it lets us study how the brain is controlling the cochlea in real time.”
The researchers genetically engineered mice to have impaired hearing, by disabling some of the nerves that carry signals from their ears to their brains. They then used OCT to monitor the activity of the cochlea, and found that it was working harder than usual.
“As humans age and our hair cells die off, we start to lose our hearing,” said Oghalai. “These findings suggest that the brain can send signals to the remaining hair cells, essentially telling them to turn up the volume.”
As useful as this mechanism might be to compensate for hearing loss, the team suggests that it might have unwanted side effects: namely, it could contribute to conditions like tinnitus. The brain cranking the cochlea’s volume could produce that annoying ringing associated with tinnitus, like the hiss you hear when turning a speaker up too loud with nothing playing.
On the positive side, the team now plans to test drugs that could block these backwards nerve fibers as a potential treatment for tinnitus, and related conditions like hyperacusis, where everyday sounds seem uncomfortably loud.
If some speakers in your sound system were broken, you might try to compensate by cranking up the volume on the ones that still work. It turns out that the brain does the same thing when damaged hair cells in the ear lead to hearing loss – and this could be causing your tinnitus.
Sensory hair cells are tiny structures in the cochlea that wave like blades of grass in the wind – but in this case, it’s the pressure of sound waves that gets them moving. When they do, they create electrical signals that are funneled through nerve fibers to the brain, to process what you’re hearing.
But a small percentage of these nerves actually run in the opposite direction, from the brain to the cochlea. Scientists have long been puzzled by the function of these backwards channels, and it’s hard to study their activity while people or animals are awake.
In the new study, scientists at the University of Southern California (USC) used an intriguing imaging tool to see what’s going on in there. The technique is called optical coherence tomography (OCT), which involves creating a 3D image of tissue using light waves. It’s currently used to scan the retina to diagnose conditions like glaucoma, but the team adapted it for use in the ear.
“OCT lets us look down the ear canal, through the eardrum and bone into the cochlea, and measure how it’s working – non-invasively and without pain,” said John Oghalai, lead author of the study. “What’s exciting about this is it lets us study how the brain is controlling the cochlea in real time.”
The researchers genetically engineered mice to have impaired hearing, by disabling some of the nerves that carry signals from their ears to their brains. They then used OCT to monitor the activity of the cochlea, and found that it was working harder than usual.
“As humans age and our hair cells die off, we start to lose our hearing,” said Oghalai. “These findings suggest that the brain can send signals to the remaining hair cells, essentially telling them to turn up the volume.”
As useful as this mechanism might be to compensate for hearing loss, the team suggests that it might have unwanted side effects: namely, it could contribute to conditions like tinnitus. The brain cranking the cochlea’s volume could produce that annoying ringing associated with tinnitus, like the hiss you hear when turning a speaker up too loud with nothing playing.
On the positive side, the team now plans to test drugs that could block these backwards nerve fibers as a potential treatment for tinnitus, and related conditions like hyperacusis, where everyday sounds seem uncomfortably loud.
