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Rare Neurons May Process Painful Noise
21 October 2009 (All day)
If your ears are still ringing from that last Metallica concert, scientists can't help you--but they may have figured out what's going on in your head. A type of small neuron in the inner ear, it seems, may help process painfully loud sounds. The discovery solves a 70-year-old mystery about what these neurons do--and may deepen understanding of hearing loss and impairment.
Humans and other mammals owe their hearing to a forest of hairlike cells in the inner ear. As sound waves move into the ear, the hair cells sway along, and their motion releases electrical and chemical signals that the brain interprets as sound.
Two kinds of neurons transmit those signals. Type I is the standard: It makes up 90% to 95% of all neurons in the inner ear and tells the brain about a sound's frequency, volume, and timing--all the ingredients of hearing as we know it. The remaining 5% of the neurons are type II, which were first described in 1937 and are smaller and harder to study. In fact, just a single study has reported success in connecting a type II neuron to an electrode, which is the main method for studying hearing cells.
Hearing researcher Paul Fuchs and his colleagues at the Johns Hopkins University School of Medicine in Baltimore, Maryland, came up with a different way to isolate the elusive neurons. Instead of trying to find them within an intact ear, they dissected the inner ears of rats. During a window of only a few hours before the tissue samples died, the researchers tracked down the type II neurons, hooked them up to electrodes, and recorded what they did in the presence of a chemical that provokes the same reaction as sound in hearing cells.
The team found that the type II neurons were indeed reacting to sound but only to very loud sound. They were also especially sensitive to ATP, a neurotransmitter associated with painful stimuli and tissue damage, among many other functions. Together, these observations suggest that the type II neurons are "a specialized pathway for very loud sound," says Fuchs, whose group reports its findings tomorrow in Nature.
A "pain pathway" role for type II neurons may also help explain why hearing loss is often accompanied by increased sensitivity to loudness and pain. By sensitizing the ear after damage has occurred, the type II fibers may be working to prevent future damage, Fuchs says.
“In one fell swoop, this study increased what we know by an order of magnitude," says Jonathan Ashmore, a cochlear physiologist at University College London. But he notes that the neurons' sensitivity to ATP could point to a different role in the ear. They may help the brain monitor whether the cochlea's hair cells are working properly or have been damaged, without actually processing the traumatic sound. In either case, the technique opens an exciting door, adds Ashmore. "We know almost nothing about the underlying neuroscience of hearing loss or impairments like tinnitus."