New Proof Touch-Sensing Nerve Cells Can Aggravate 'Ringing In the Ears'

by Nancy Needhima on  February 3, 2012 at 11:27 PM Research News   - G J E 4
It's a common experience when it takes a little while for our hearing to be restored after listening to our iPods too loud or attending a raucous concert.But new research at the University of Michigan Health System suggests over-exposure to noise can actually cause more lasting changes to our auditory circuitry - changes that may lead to tinnitus, commonly known as ringing in the ears.
New Proof Touch-Sensing Nerve Cells Can Aggravate 'Ringing In the Ears'
New Proof Touch-Sensing Nerve Cells Can Aggravate 'Ringing In the Ears'

U-M researchers previously demonstrated that after hearing damage, touch-sensing "somatosensory" nerves in the face and neck can become overactive, seeming to overcompensate for the loss of auditory input in a way the brain interprets - or "hears" - as noise that isn't really there.

The new study, which appears in the Feb. 1 issue of The Journal of Neuroscience, found that somatosensory neurons maintain a high level of activity following exposure to loud noise, even after hearing itself returns to normal.

The findings were made in guinea pigs, but mark an important step toward potential relief for people plagued by tinnitus, says lead investigator Susan E. Shore, Ph.D., of U-M's Kresge Hearing Research Institute and a professor of otolaryngology and molecular and integrative physiology at the U-M Medical School.

"The animals that developed tinnitus after a temporary loss in their hearing after loud noise exposure were the ones who had sustained increases in activity in these neural pathways," Shore says. "In the future it may be possible to treat tinnitus patients by dampening the hyperactivity by reprogramming these auditory-touch circuits in the brain."

In normal hearing, a part of the brain called the dorsal cochlear nucleus is the first stop for signals arriving from the ear via the auditory nerve. But it's also a hub where "multitasking" neurons process other sensory signals, such as touch, together with hearing information.

During hearing loss, the other sensory signals entering the dorsal cochlear nucleus are amplified, Shore's earlier research found. This overcompensation by the somatosensory neurons, which carry information about touch, vibration, skin temperature and pain, is believed to fuel tinnitus in many cases.

Tinnitus affects up to 50 million people in the United States and millions more worldwide, according to the American Tinnitus Association. It can range from intermittent and mildly annoying to chronic, severe and debilitating. There is no cure.

Source: Eurekalert

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