Research reveals that temporary hearing deprivation can lead to 'lazy ear'

听到科学家丹尼尔·波莉investi博士gator at Massachusetts Eye and Ear Infirmary's Eaton-Peabody Laboratories of Auditory Physiology, has gained new insight into why a relatively short-term hearing deprivation during childhood may lead to persistent hearing deficits, long after hearing is restored to normal. The research, featured on the cover on the March 11 issue of the journalNeuron, reveals that, much like the visual cortex, development of the auditory cortex is quite vulnerable if it does not receive appropriate stimulation at just the right time.

It is well established that degraded sensory experience during critical periods of childhood development can have detrimental effects on the brain and behavior. In the classic example, a condition called amblyopia (also known as lazy eye) can arise when balanced visual signals are not transmitted from each eye to the brain during a critical period forvisual cortexdevelopment.

"An analogous problem may exist in the realm of hearing, in that children commonly experience a buildup of viscous fluid in the middle ear cavity which can degrade the quality of acoustic signals reaching the brain, which has been associated with a long-lasting loss of auditory perceptual acuity," explains senior study author, Dr. Polley.

Dr. Polley and his colleague Dr. Maria Popescu from Vanderbilt University implemented a method to reversibly block hearing in one ear in infant, juvenile and adult rats then looked at how the parts of the brain involved in hearing were impacted by the temporary hearing loss.

They observed that the temporary hearing loss in one ear distorted auditory patterning in the brain, weakened the deprived ear's representation and strengthened the open ear's representation. The scope of reorganization was most striking in the cortex (and not "lower" parts of the central auditory pathways) and was more pronounced when hearing deprivation began in infancy than in later life. Therefore, it appears that maladaptive plasticity in the developingauditory cortexmight underlie "amblyaudio," in a similar fashion to the contributions of visual cortex plasticity to amblyopia.

"The good news about amblyaudio is that it is unlikely to be a permanent problem for most people," concludes Dr. Polley. "Even if theacoustic signalisn't corrected within the critical period, the mature auditory cortex still expresses a remarkable degree of plasticity. We know that properly designed visual training can improve visual acuity in adultamblyopiapatients. We are gearing up now to study whether auditory perceptual training may also be a promising approach to accelerate recovery in individuals with unresolved auditory processing deficits stemming from childhood hearing loss."