That area, called the dorsal cochlear nucleus, is the first station for signals arriving in the brain from the ear via the auditory nerve. But it's also a center where "multitasking" neurons integrate other sensory signals, such as touch, together with the hearing information.
In tinnitus, some of the input to the brain from the ear's cochlea is reduced, while signals from the somato-sensory nerves of the face and neck, related to touch, are excessively amplified.
Susan Shore, Ph.D., the senior author of the paper, explains that her team has confirmed that a process called stimulus-timing dependent multisensory plasticity is altered in animals with tinnitus -- and that this plasticity is "exquisitely sensitive" to the timing of signals coming in to a key area of the brain. It's as if the signals are compensating for the lost auditory input, but they overcompensate and end up making everything noisy," says Shore.
The new findings illuminate the relationship between tinnitus, hearing loss and sensory input and help explain why many tinnitus sufferers can change the volume and pitch of their tinnitus's sound by clenching their jaw, or moving their head and neck. But it's not just the combination of loud noise and overactive somatosensory signals that are involved in tinnitus, its the precise timing of these signals in relation to one another that prompt the changes in the nervous system's plasticity mechanisms, which may lead to the symptoms known to tinnitus sufferers.
In tinnitus, some of the input to the brain from the ear's cochlea is reduced, while signals from the somato-sensory nerves of the face and neck, related to touch, are excessively amplified.
Susan Shore, Ph.D., the senior author of the paper, explains that her team has confirmed that a process called stimulus-timing dependent multisensory plasticity is altered in animals with tinnitus -- and that this plasticity is "exquisitely sensitive" to the timing of signals coming in to a key area of the brain. It's as if the signals are compensating for the lost auditory input, but they overcompensate and end up making everything noisy," says Shore.
The new findings illuminate the relationship between tinnitus, hearing loss and sensory input and help explain why many tinnitus sufferers can change the volume and pitch of their tinnitus's sound by clenching their jaw, or moving their head and neck. But it's not just the combination of loud noise and overactive somatosensory signals that are involved in tinnitus, its the precise timing of these signals in relation to one another that prompt the changes in the nervous system's plasticity mechanisms, which may lead to the symptoms known to tinnitus sufferers.
In this study, only half of the animals receiving a noise-overexposure developed tinnitus. This is similarly the case with humans -- not everyone with hearing damage ends up with tinnitus. An important finding in the new paper is that animals that did not get tinnitus showed fewer changes in their multisensory plasticity than those with evidence of tinnitus. In other words, their neurons were not hyperactive.
Shore is now working with other students and postdoctoral fellows to develop a device that uses the new knowledge about the importance of signal timing to alleviate tinnitus. The device will combine sound and electrical stimulation of the face and neck in order to return to normal the neural activity in the auditory pathway.
"If we get the timing right, we believe we can decrease the firing rates of neurons at the tinnitus frequency, and target those with hyperactivity," says Shore. She and her colleagues are also working to develop pharmacological manipulations that could enhance stimulus timed plasticity by changing specific molecular targets.
Ref:
- Seth D. Koehler And Susan E. Shore. Stimulus Timing-Dependent Plasticity in Dorsal Cochlear Nucleus Is Altered in Tinnitus. Journal of Neuroscience, December 2013
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