Posts tagged noise exposure
Articles and news from the latest research reports.
Pitt team finds mechanism that causes noise-induced tinnitus and drug that can prevent it
An epilepsy drug shows promise in an animal model at preventing tinnitus from developing after exposure to loud noise, according to a new study by researchers at the University of Pittsburgh School of Medicine. The findings, reported this week in the early online version of the Proceedings of the National Academy of Sciences, reveal for the first time the reason the chronic and sometimes debilitating condition occurs.
An estimated 5 to 15 percent of Americans hear whistling, clicking, roaring and other phantom sounds of tinnitus, which typically is induced by exposure to very loud noise, said senior investigator Thanos Tzounopoulos, Ph.D., associate professor and member of the auditory research group in the Department of Otolaryngology, Pitt School of Medicine.
"There is no cure for it, and current therapies such as hearing aids don’t provide relief for many patients," he said. "We hope that by identifying the underlying cause, we can develop effective interventions."
The team focused on an area of the brain that is home to an important auditory center called the dorsal cochlear nucleus (DCN). From previous research in a mouse model, they knew that tinnitus is associated with hyperactivity of DCN cells — they fire impulses even when there is no actual sound to perceive. For the new experiments, they took a close look at the biophysical properties of tiny channels, called KCNQ channels, through which potassium ions travel in and out of the cell.
"We found that mice with tinnitus have hyperactive DCN cells because of a reduction in KCNQ potassium channel activity," Dr. Tzounopoulos said. "These KCNQ channels act as effective "brakes" that reduce excitability or activity of neuronal cells."
In the model, sedated mice are exposed in one ear to a 116-decibel sound, about the loudness of an ambulance siren, for 45 minutes, which was shown in previous work to lead to the development of tinnitus in 50 percent of exposed mice. Dr. Tzounopoulos and his team tested whether an FDA-approved epilepsy drug called retigabine, which specifically enhances KCNQ channel activity, could prevent the development of tinnitus. Thirty minutes into the noise exposure and twice daily for the next five days, half of the exposed group was given injections of retigabine.
Seven days after noise exposure, the team determined whether the mice had developed tinnitus by conducting startle experiments, in which a continuous, 70 dB tone is played for a period, then stopped briefly and then resumed before being interrupted with a much louder pulse. Mice with normal hearing perceive the gap in sounds and are aware something had changed, so they are less startled by the loud pulse than mice with tinnitus, which hear phantom noise that masks the moment of silence in between the background tones.
The researchers found that mice that were treated with retigabine immediately after noise exposure did not develop tinnitus. Consistent with previous studies, 50 percent of noise-exposed mice that were not treated with the drug exhibited behavioral signs of the condition.
"This is an important finding that links the biophysical properties of a potassium channel with the perception of a phantom sound," Dr. Tzounopoulos said. "Tinnitus is a channelopathy, and these KCNQ channels represent a novel target for developing drugs that block the induction of tinnitus in humans."
The KCNQ family is comprised of five different subunits, four of which are sensitive to retigabine. He and his collaborators aim to develop a drug that is specific for the two KCNQ subunits involved in tinnitus to minimize the potential for side effects.
"Such a medication could be a very helpful preventive strategy for soldiers and other people who work in situations where exposure to very loud noise is likely," Dr. Tzounopoulos said. "It might also be useful for other conditions of phantom perceptions, such as pain in a limb that has been amputated."
(Source: eurekalert.org)
![New understanding of hearing loss
A major breakthrough in the understanding of hearing and noise-induced hearing loss has been made by hearing scientists from three Pacific Rim universities.
Scientists from The University of Auckland, the University of New South Wales in Sydney, and the University of California in San Diego have collaborated for nearly 20 years on this research.
“This work represents a paradigm shift in understanding how our ears respond to noise exposure,” says Professor Peter Thorne from The University of Auckland, who is one of the co-authors of two papers published recently in the prestigious journal, the Proceedings of the National Academy of Sciences (PNAS) [1, 2].
“We demonstrate that what we traditionally regard as a temporary hearing loss from noise exposure is in fact the cochlea of the inner ear adapting to the noisy environment, turning itself down in order to be able to detect new signals that appear in the noise,” he says.
After the noise is turned off, hearing remains temporarily dull for some time while it readjusts to the lack of noise.
“Clinically, this is what we measure as a temporary hearing loss,” says Professor Thorne. “This has always been regarded as an indication of noise damage rather than, in our new view, a normal physiological process.”
The researchers show that this is due to a molecular signalling pathway in the cochlea, mediated by a chemical compound called ATP, released by the cochlear tissue with noise and activating specific ATP receptors in the cochlear cells.
“Interestingly, if the pathway is removed, such as by genetic manipulations, this adaptive mechanism doesn’t occur and the ear becomes very vulnerable to longer term noise exposure and the effects of age, eventually resulting in permanent hearing loss.”
“In other words the adaptive mechanism also protects the ear,” says Professor Thorne.
The second paper, done in collaboration with United States colleagues, reveals a new genetic cause of deafness in humans which involves exactly the same mechanism.
People (two families in China) who had a mutation in the ATP receptor showed a rapidly progressing hearing loss which was accelerated if they worked in noisy environments.
“This work is important because it shows that our ears naturally adapt to their environment, a bit like pupils of the eye which dilate or constrict with light, but over a longer time course,” Professor Thorne says.
This inherent adaptive process also provides protection to the ear from noise and age-related wear and tear. If people don’t have the genes that produce this protection, then they are more likely susceptible to developing hearing loss.
“This may go some way to explaining why some people are very vulnerable to noise or develop hearing loss with age and others don’t,” he says.
“Our research demonstrates that what we have always thought was temporary noise damage (i.e. the temporary hearing loss experienced in night clubs or a day’s work in factories), may not be this, but instead, is the ear regulating its sensitivity in background noise”.
“Although our research suggests that our hearing adapts in some noise environments, this has limits,” says Professor Thorne. “If we exceed the safe dose of noise, our ears can still be damaged permanently despite this apparent protective mechanism.”
“People need to protect their ears from constant noise exposure to prevent hearing loss and this is particularly important in the workplace and with personal music devices which can deliver high sound levels for long periods of time,” he says.](http://40.media.tumblr.com/a9756dde50c0fbfe31ffa8f00f989a63/tumblr_mljr5rIDfB1rog5d1o1_500.jpg)
New understanding of hearing loss
A major breakthrough in the understanding of hearing and noise-induced hearing loss has been made by hearing scientists from three Pacific Rim universities.
Scientists from The University of Auckland, the University of New South Wales in Sydney, and the University of California in San Diego have collaborated for nearly 20 years on this research.
“This work represents a paradigm shift in understanding how our ears respond to noise exposure,” says Professor Peter Thorne from The University of Auckland, who is one of the co-authors of two papers published recently in the prestigious journal, the Proceedings of the National Academy of Sciences (PNAS) [1, 2].
“We demonstrate that what we traditionally regard as a temporary hearing loss from noise exposure is in fact the cochlea of the inner ear adapting to the noisy environment, turning itself down in order to be able to detect new signals that appear in the noise,” he says.
After the noise is turned off, hearing remains temporarily dull for some time while it readjusts to the lack of noise.
“Clinically, this is what we measure as a temporary hearing loss,” says Professor Thorne. “This has always been regarded as an indication of noise damage rather than, in our new view, a normal physiological process.”
The researchers show that this is due to a molecular signalling pathway in the cochlea, mediated by a chemical compound called ATP, released by the cochlear tissue with noise and activating specific ATP receptors in the cochlear cells.
“Interestingly, if the pathway is removed, such as by genetic manipulations, this adaptive mechanism doesn’t occur and the ear becomes very vulnerable to longer term noise exposure and the effects of age, eventually resulting in permanent hearing loss.”
“In other words the adaptive mechanism also protects the ear,” says Professor Thorne.
The second paper, done in collaboration with United States colleagues, reveals a new genetic cause of deafness in humans which involves exactly the same mechanism.
People (two families in China) who had a mutation in the ATP receptor showed a rapidly progressing hearing loss which was accelerated if they worked in noisy environments.
“This work is important because it shows that our ears naturally adapt to their environment, a bit like pupils of the eye which dilate or constrict with light, but over a longer time course,” Professor Thorne says.
This inherent adaptive process also provides protection to the ear from noise and age-related wear and tear. If people don’t have the genes that produce this protection, then they are more likely susceptible to developing hearing loss.
“This may go some way to explaining why some people are very vulnerable to noise or develop hearing loss with age and others don’t,” he says.
“Our research demonstrates that what we have always thought was temporary noise damage (i.e. the temporary hearing loss experienced in night clubs or a day’s work in factories), may not be this, but instead, is the ear regulating its sensitivity in background noise”.
“Although our research suggests that our hearing adapts in some noise environments, this has limits,” says Professor Thorne. “If we exceed the safe dose of noise, our ears can still be damaged permanently despite this apparent protective mechanism.”
“People need to protect their ears from constant noise exposure to prevent hearing loss and this is particularly important in the workplace and with personal music devices which can deliver high sound levels for long periods of time,” he says.