Enriched Acoustic Environment After Noise Trauma

Enriched acoustic environment after noise trauma abolishes neural signs of tinnitus.

Neuroreport. 2006 Apr 24;17(6):559-63.
Noreña AJ1, Eggermont JJ.
Author information

Abstract
Noise-induced hearing loss induces reorganization of the tonotopic map in cat auditory cortex and increases spontaneous firing rate and neural synchrony. We showed previously that keeping cats after noise trauma in an acoustic environment enriched in high frequencies prevents tonotopic map reorganization. Here, we show the effects of low-frequency and high-frequency enriched acoustic environments on spontaneous firing rate and neural synchrony. Exposed cats placed in the quiet environment and in the low-frequency enriched acoustic environment showed increased spontaneous firing rate and synchrony of firing. In contrast, exposed cats placed in the high-frequency enriched acoustic environment did not show significant differences in spontaneous firing rate or synchrony compared with normal hearing controls. This is interpreted as an absence of putative neural signs of tinnitus.

-

Enriched acoustic environment after noise trauma reduces hearing loss and prevents cortical map reorganization.

Noreña AJ, et al. J Neurosci. 2005.

Abstract
Exposure to sound of sufficient duration and level causes permanent damage to the peripheral auditory system, which results in the reorganization of the cortical tonotopic map. The changes are such that neurons with pre-exposure tuning to frequencies in the hearing loss range now become tuned to frequencies near the near-normal lower boundary of the hearing loss range, which thus becomes over represented. However, cats exposed to a traumatizing noise and immediately thereafter placed for a few weeks in an enriched acoustic environment presented a much-restricted hearing loss compared with similarly exposed cats that were placed for the same time in a quiet environment. The enriched environment spectrally matched the expected hearing loss range and was approximately 40 dB above the level of the expected hearing loss. The hearing loss in the quiet environment-reared cats ranged from 6 to 32 kHz with the largest loss (on average, 40 dB) ranging from 24 to 32 kHz. In contrast, the hearing loss in the enriched-environment cats was restricted to 6-8 kHz at a level of, on average, 35 dB and with 16-32 kHz having normal thresholds. Despite the remaining hearing loss for the enriched-environment cats in the 6-8 kHz range, plastic tonotopic map changes in primary auditory cortex could no longer be demonstrated, suggesting that the enriched acoustic environment prevents this reorganization. This finding has implications for the treatment of hearing disorders, such as tinnitus, that have been linked to cortical tonotopic map reorganization.

-

Noise Trauma-Induced Behavioral Gap Detection Deficits Correlate with Reorganization of Excitatory and Inhibitory Local Circuits in the Inferior Colliculus and Are Prevented by Acoustic Enrichment.

Sturm JJ, et al. J Neurosci. 2017.

Abstract
Hearing loss leads to a host of cellular and synaptic changes in auditory brain areas that are thought to give rise to auditory perception deficits such as temporal processing impairments, hyperacusis, and tinnitus. However, little is known about possible changes in synaptic circuit connectivity that may underlie these hearing deficits. Here, we show that mild hearing loss as a result of brief noise exposure leads to a pronounced reorganization of local excitatory and inhibitory circuits in the mouse inferior colliculus. The exact nature of these reorganizations correlated with the presence or absence of the animals' impairments in detecting brief sound gaps, a commonly used behavioral sign for tinnitus in animal models. Mice with gap detection deficits (GDDs) showed a shift in the balance of synaptic excitation and inhibition that was present in both glutamatergic and GABAergic neurons, whereas mice without GDDs showed stable excitation-inhibition balances. Acoustic enrichment (AE) with moderate intensity, pulsed white noise immediately after noise trauma prevented both circuit reorganization and GDDs, raising the possibility of using AE immediately after cochlear damage to prevent or alleviate the emergence of central auditory processing deficits.SIGNIFICANCE STATEMENT Noise overexposure is a major cause of central auditory processing disorders, including tinnitus, yet the changes in synaptic connectivity underlying these disorders remain poorly understood. Here, we find that brief noise overexposure leads to distinct reorganizations of excitatory and inhibitory synaptic inputs onto glutamatergic and GABAergic neurons and that the nature of these reorganizations correlates with animals' impairments in detecting brief sound gaps, which is often considered a sign of tinnitus. Acoustic enrichment immediately after noise trauma prevents circuit reorganizations and gap detection deficits, highlighting the potential for using sound therapy soon after cochlear damage to prevent the development of central processing deficits.


-

The complete studies are attached.