Augmented Acoustic Environment Research Articles

Effect of Environment-Related Cues on Auditory Distance Perception in the Context of Audio-Only Augmented Reality

Audio-only augmented reality consists of enhancing a real environment with virtual sound events. A seamless integration of the virtual events within the environment requires processing them with artificial spatialization and reverberation effects that simulate the acoustic properties of the room. However, in augmented reality, the visual and acoustic environment of the listener may not be fully mastered. This study aims to gain some insight into the acoustic cues (intensity and reverberation) that are used by the listener to form an auditory distance judgment, and to observe if these strategies can be influenced by the listener’s environment. To do so, we present a perceptual evaluation of two distance-rendering models informed by a measured Spatial Room Impulse Response. The choice of the rendering methods was made to design stimuli categories in which the availability and reproduction quality of acoustic cues are different. The proposed models have been evaluated in an online experiment gathering 108 participants who were asked to provide judgments of auditory distance about a stationary source. To evaluate the importance of environmental cues, participants had to describe the environment in which they were running the experiment, and more specifically the volume of the room and the distance to the wall they were facing. It could be shown that these context cues had a limited, but significant, influence on the perceived auditory distance.

Rescuing Auditory Temporal Processing with a Novel Augmented Acoustic Environment in an Animal Model of Congenital Hearing Loss.

Congenital sensorineural hearing loss (SNHL) affects thousands of infants each year and results in significant delays in speech and language development. Previous studies have shown that early exposure to a simple augmented acoustic environment (AAE) can limit the effects of progressive SNHL on hearing sensitivity. However, SNHL is also accompanied by hearing loss that is not assessed on standard audiological examinations, such as reduced temporal processing acuity. To assess whether sound therapy may improve these deficits, a mouse model of congenital SNHL was exposed to simple or temporally complex AAE. The DBA/2J mouse strain develops rapid, base to apex, progressive SNHL beginning at birth and is functionally deaf by six months of age. Hearing sensitivity and auditory brainstem function was measured using otoacoustic emissions, auditory brainstem response (ABR) and extracellular recording from the inferior colliculus (IC) in mice following exposure to 30 d of continuous AAE. Peripheral function and sound sensitivity in auditory midbrain neurons improved following exposure to both types of AAE. However, exposure to a novel, temporally complex AAE more strongly improved a measure of temporal processing acuity, neural gap-in-noise detection in the auditory midbrain. These experiments suggest that targeted sound therapy may be harnessed to improve hearing outcomes for children suffering from congenital SNHL.

Auditory stimulation modulates CXCL12/CXCR4 expression in postnatal development of the newborn rat cochlea.

Sensorineural hearing loss is one of the most common sensory deficits. Recently, inner-ear stem cell therapy has been proposed for auditory afferent rehabilitation. CXCR4 is the primary physiologic receptor for CXC chemokine ligand 12 (CXCL12) and the CXCL12-CXCR4 pathway has been implicated in the process of migration, differentiation, and maturation of vertebrate neural stem cells. In this study, we examined changes in the auditory brainstem response and CXCL12/CXCR4 expression in newborn rat cochleae under different acoustic environments by quantitative real-time PCR, western blot, enzyme-linked immunosorbent assay, immunohistochemistry, and immunofluorescence analyses. Rats were divided randomly into three groups: the augmented acoustic environment (AAE) group, the auditory deprivation (AD) group, and the control group. Auditory brainstem response thresholds were markedly increased in the AAE group and in the AD group. Compared with postnatal day 1, the expression of CXCL12/CXCR4 mRNA and protein under normal acoustic conditions was increased on postnatal day 14 and then decreased on postnatal day 28 in the cochlea. However, on postnatal day 28, CXCL12/CXCR4 expression, as well as its spatiotemporal distribution as detected by immunohistochemistry and immunofluorescence assays, was augmented by AAE treatment and inhibited by AD treatment. Therefore, our results confirmed that auditory stimulation influenced the spatiotemporal expression of CXCL12/CXCR4 in newborn rat cochlea, which might help to unravel the role of the CXCL12-CXCR4 pathway in the synaptic contacts and hearing function establishment in rat cochlea development.

Exposure to acoustic stimuli promotes the development and differentiation of neural stem cells from the cochlear nuclei through the clusterin pathway.

Stem cell therapy has attracted widespread attention for a number of diseases. Recently, neural stem cells (NSCs) from the cochlear nuclei have been identified, indicating a potential direction for the treatment of sensorineural hearing loss. Acoustic stimuli play an important role in the development of the auditory system. In this study, we aimed to determine whether acoustic stimuli induce NSC development and differentiation through the upregulation of clusterin (CLU) in NSCs isolated from the cochlear nuclei. To further clarify the underlying mechanisms involved in the development and differentiation of NSCs exposed to acoustic stimuli, we successfully constructed animal models in which was CLU silenced by an intraperitoneal injection of shRNA targeting CLI. As expected, the NSCs from rats treated with LV-CLU shRNA exhibited a lower proliferation ratio when exposed to an augmented acoustic environment (AAE). Furthermore, the inhibition of cell apoptosis induced by exposure to AAE was abrogated after silencing the expression of the CLU gene. During the differentiation of acoustic stimuli-exposed stem cells into neurons, the number of astrocytes was significantly reduced, as evidenced by the expression of the cell markers, microtubule associated protein-2 (MAP-2) and glial fibrillary acidic protein (GFAP), which was markedly inhibited when the CLU gene was silenced. Our results indicate that acoustic stimuli may induce the development and differentiation of NSCs from the cochlear nucleus mainly through the CLU pathway. Our study suggests that CLU may be a novel target for the treatment of sensorineural hearing loss.

Mutation in Osteoactivin Decreases Bone Formation in Vivo and Osteoblast Differentiation in Vitro

We have previously identified osteoactivin (OA), encoded by Gpnmb, as an osteogenic factor that stimulates osteoblast differentiation invitro. To elucidate the importance of OA in osteogenesis, we characterized the skeletal phenotype of a mouse model, DBA/2J (D2J) with a loss-of-function mutation in Gpnmb. Microtomography of D2J mice showed decreased trabecular mass, compared to that in wild-type mice [DBA/2J-Gpnmb(+)/SjJ (D2J/Gpnmb(+))]. Serum analysis showed decreases in OA and the bone-formation markers alkaline phosphatase and osteocalcin in D2J mice. Although D2J mice showed decreased osteoid and mineralization surfaces, their osteoblasts were increased in number, compared to D2J/Gpnmb(+) mice. We then examined the ability of D2J osteoblasts to differentiate in culture, where their differentiation and function were decreased, as evidenced by low alkaline phosphatase activity and matrix mineralization. Quantitative RT-PCR analyses confirmed the decreased expression of differentiation markers in D2J osteoblasts. Invitro, D2J osteoblasts proliferated and survived significantly less, compared to D2J/Gpnmb(+) osteoblasts. Next, we investigated whether mutant OA protein induces endoplasmic reticulum stress in D2J osteoblasts. Neither endoplasmic reticulum stress markers nor endoplasmic reticulum ultrastructure were altered in D2J osteoblasts. Finally, we assessed underlying mechanisms that might alter proliferation of D2J osteoblasts. Interestingly, TGF-β receptors and Smad-2/3 phosphorylation were up-regulated in D2J osteoblasts, suggesting that OA contributes to TGF-β signaling. These data confirm the anabolic role of OA in postnatal bone formation.

Acoustical stimulus changes the expression of stromal cell-derived factor-1 in the spiral ganglion neurons of the rat cochlea

Neural stem cell (NSC) transplantation into the cochlea has been tested as a treatment for spiral ganglion neuron (SGN) degenerative disease and injury in various animal models. A recent study has shown evidence of functional recovery after transplantation of the stem cells into a degenerated-SGN model. Chemokine stromal cell-derived factor-1 (SDF-1, or known as CXC chemokine ligand-12, CXCL-12) signaling through CXCR4 has previously been identified as a key step in the homing of the stem cells within the injury areas; meanwhile, studies have revealed that the SDF-1/CXCR4 axis is also involved in axon guidance and pathfinding. A study found that transplanted neural precursor cells can migrate to the root of the auditory nerve when animals are subjected to an augmented acoustic environment (AAE). In accordance with these studies, we hypothesize that AAE will up-regulate the expression of SDF-1 in acoustic nerves. We tested our hypothesis by examining the expression of SDF-1 in different acoustic environments, and the results were confirmed by the auditory brainstem response (ABR), immunohistochemical and RT-PCR analyses. The results showed that SDF-1 was expressed at a relatively low level in the SGNs under normal animal unit acoustic conditions (40–50dB). Moreover, it was significantly up-regulated in the SGNs under the 75dB (augmented physiological process without hearing loss) and 90dB AAE (pathological process with light hearing loss) conditions; however, under the 115dB AAE (pathological process with severe hearing loss) condition, the expression of SDF-1 was not up-regulated. The results confirmed that appropriately augmented acoustical stimuli lead to the up-regulation of SDF-1, which may assist in the migration of the transplanted cells and the subsequent establishment of essential synaptic contacts between the exogenous cells and the host auditory pathway.

Acoustic Experience Alters the Aged Auditory System

Presbyacusis, one of the most common ailments of the elderly, is often treated with hearing aids, which serve to reintroduce some or all of those sounds lost to peripheral hearing loss. However, little is known about the underlying changes to the ear and brain as a result of such experience with sound late in life. The present study attempts to model this process by rearing aged CBA mice in an augmented acoustic environment (AAE). Aged (22-23 months) male (n = 12) and female (n = 9) CBA/CaJ mice were reared in either 6 weeks of low-level (70 dB SPL) broadband noise stimulation (AAE) or normal vivarium conditions. Changes as a function of the treatment were measured for behavior, auditory brainstem response thresholds, hair cell cochleograms, and gamma aminobutyric acid neurochemistry in the key central auditory structures of the inferior colliculus and primary auditory cortex. The AAE-exposed group was associated with sex-specific changes in cochlear pathology, auditory brainstem response thresholds, and gamma aminobutyric acid neurochemistry. Males exhibited significantly better thresholds and reduced hair cell loss (relative to controls) whereas females exhibited the opposite effect. AAE was associated with increased glutamic acid decarboxylase (GAD67) levels in the inferior colliculus of both male and female mice. However, in primary auditory cortex AAE exposure was associated with increased GAD67 labeling in females and decreased GAD67 in males. These findings suggest that exposing aged mice to a low-level AAE alters both peripheral and central properties of the auditory system and these changes partially interact with sex or the degree of hearing loss before AAE. Although direct application of these findings to hearing aid use or auditory training in aged humans would be premature, the results do begin to provide direct evidence for the underlying changes that might be occurring as a result of hearing aid use late in life. These results suggest the aged brain retains significantly anatomical, electrophysiological, and neurochemical plasticity.

Persistent effects of early augmented acoustic environment on the auditory brainstem

Acoustic experiences significantly shape the functional organization of the auditory cortex during postnatal "critical periods." Here, we investigate the effects of a non-traumatic augmented acoustic environment (AAE) on the central nucleus of the inferior colliculus (ICC) and lower brainstem nuclei in rat during the critical period. Our results show that an AAE during P9-P28 had a persistent effect on the evoked auditory brainstem responses leading to a decreased latency and an increased amplitude of the response at and above the frequency of the stimulus used for the AAE. These findings are correlated with increased numbers of sites in the ICC that responded to the AAE frequency and show higher thresholds. There also were persistent effects in neurons with a best frequency higher than the AAE stimulus. These neurons showed decreased activity at low sound levels in the low frequency tail of the frequency response area. This was at, below and above the AAE stimulus frequency. Less often, increased activity at higher sound levels also was seen. Together, these findings suggest multifaceted interactions between activity-dependent plasticity, homeostasis, and development in the brainstem during the initial stages of hearing. A neonate exposed to an altered auditory environment may experience long-lasting change over the entire network of the auditory system.

Effects of a high-frequency augmented acoustic environment on parvalbumin immunolabeling in the anteroventral cochlear nucleus of DBA/2J and C57BL/6J mice

Neurons in the anteroventral cochlear nucleus (AVCN) of DBA/2J (D2) and C57BL/6J (B6) mice were immunohistochemically labeled for the calcium binding protein parvalbumin (PV). Prior to this, mice were treated for 12 h nightly with a “high-frequency” augmented acoustic environment (HAAE: repetitive bursts of a 70 dB sound pressure level, half-octave noise band centered at 20 kHz). This was done during the period that hearing loss occurs: pre-weaning to 55 days in D2 mice and weaning to 9 months in B6 mice. After HAAE treatment in D2 mice, high-frequency hearing loss was ameliorated and fewer PV-labeled neurons were found in the AVCN compared to untreated controls. HAAE treatment in B6 mice exacerbated high-frequency hearing loss, yet the number of PV-labeled AVCN neurons in treated mice did not differ significantly from that of control mice. The findings suggest that HAAE treatment provides relief from physiological stress caused by deprivation of auditory input from the impaired cochlea.

Age-related hearing loss: Is it a preventable condition?

Numerous techniques have been tested to attempt to prevent the onset or progression of age-related hearing loss (ARHL): raising the animals in an augmented acoustic environment (used successfully in mouse and rat models), enhancing the antioxidant defenses with exogenous antioxidant treatments (used with mixed results in mouse and rat models), raising the animals with a calorie restricted diet (used successfully in mouse and rat models), restoring lost endocochlear potential voltage with exogenous electrical stimulation (used successfully in the Mongolian gerbil model), and hypothetical enhancement of outer hair cell electromotility with salicylate therapy. Studies of human ARHL have revealed a set of unique hearing loss configurations with unique underlying pathologies. Animal research has developed models for the different forms of age-related peripheral pathology. Using the animal models, different techniques for prevention of ARHL have been developed and tested. The current review discusses ARHL patterns in humans and animal models, followed by discussions of the different prevention techniques.

Ameliorative effects of an augmented acoustic environment on age‐related hearing loss in middle‐aged Fischer 344/NHsd rats

To investigate the effects of an augmented acoustic environment (AAE) on age-related hearing loss (ARHL) and outer hair cell (OHC) pathology in middle-aged Fischer 344/NHsd (F344/NHsd) rats. Eleven F344/NHsd rats were divided into two groups: 1) the AAE group (n = 5), which was exposed to 4-20 kHz broadband noise at 80 dB SPL for 12 h/d, 5 d/wk for 13 weeks starting from 16 months of age; and 2) the control group (n = 6), which did not receive the AAE during the same time span. Auditory brainstem response thresholds were obtained at different time points, and OHC pathology was examined after 13 weeks of AAE using propidium iodide and antiprestin antibody staining. The AAE-treated rats showed smaller mean threshold shifts (-1 to -3 dB) at 20-40 kHz than the control group (7.5-16.7 dB) at 13 weeks. No significant group differences were observed in the percentage of missing OHCs or abnormal OHC nuclei. However, examination of prestin in a pair of AAE and control rats revealed more uniform prestin staining intensity among OHCs in the AAE-treated cochlea than in the control cochlea. Thirteen-week AAE treatment in the middle-aged F344/NHsd rats slowed progression of ARHL. The AAE did not show a significant effect on OHC degeneration, but it is speculated that the AAE may maintain the integrity of prestin to preserve OHC functionality. However, further study is warranted to understand the protective mechanism of AAE as an intervention against ARHL.

The effects of acoustic environment after traumatic noise exposure on hearing and outer hair cells

Previous studies reported that exposure to non-traumatic level sounds after traumatic noise exposure reduced the degree of noise-induced hearing loss and hair cell stereocilia damage. The current study investigated the effects of a 3-day post-noise acoustic environment on the degree of noise-induced hearing loss and cochlear damage. Female chinchillas were exposed to traumatic continuous noise (4 kHz octave-band noise) at 107 dB SPL for 1 h and then placed in either an augmented acoustic environment (AAE) or deprived acoustic environment (DAE) for 3 days. The AAE group was exposed to a broad-band noise (4–20 kHz) at 80 dB SPL and the DAE animals were fit with conventional earplugs to minimize the level of acoustic stimulation. Auditory brainstem responses (ABRs) were recorded before and 3 days after the traumatic noise exposure. The AAE group showed a significantly lower average threshold shift at the frequencies of 4 and 8 kHz ( p < 0.01). Correspondingly, significantly fewer missing and dying outer hair cells (OHCs) were observed in the AAE group than in the DAE group. Although the cochlear reduced and oxidized glutathione levels (GSH and GSSG, respectively) were essentially the same in two groups at day 3, significant correlations were found between GSSG levels and mean ABR threshold shift (1–16 kHz) in the AAE group; as well as GSSG and percentage of total OHC loss in the DAE group. The results suggest that post-noise acoustic environment influenced the degree of hearing loss and OHC deterioration after traumatic noise exposure.

Mecanismos de plasticidad (funcional y dependiente de actividad) en el cerebro auditivo adulto y en desarrollo

Sensory systems show a topographic representation of the sensory epithelium in the central nervous system. In the auditory system this representation originates tonotopic maps. For the last four decades these changes in tonotopic maps have been widely studied either after peripheral mechanical lesions or by exposing animals to an augmented acoustic environment. These sensory manipulations induce plastic reorganizations in the tonotopic map of the auditory cortex. By contrast, acoustic trauma does not seem to induce functional plasticity at subcortical nuclei. Mechanisms that generate these changes differ in their molecular basis and temporal course and we can distinguish two different mechanisms: those involving an active reorganization process, and those that show a simple reflection of the loss of peripheral afferences. Only the former involve a genuine process of plastic reorganization. Neuronal plasticity is critical for the normal development and function of the adult auditory system, as well as for the rehabilitation needed after the implantation of auditory prostheses. However, development of plasticity can also generate abnormal sensation-like tinnitus. Recently, a new concept in neurobiology so-called 'neuronal stability' has emerged and its implications and conceptual basis could help to improve the treatments of hearing loss. A combination of neuronal plasticity and stability is suggested as a powerful and promising future strategy in the design of new treatments of hearing loss.

Effects of exposing C57BL/6J mice to high- and low-frequency augmented acoustic environments: Auditory brainstem response thresholds, cytocochleograms, anterior cochlear nucleus morphology and the role of gonadal hormones

Gonadectomized and intact adult C57BL/6J (B6) mice of both sexes were exposed for 12 h nightly to an augmented acoustic environment (AAE): repetitive bursts of a 70 dB SPL noise band. The high-frequency AAE (HAAE) was a half-octave band centered at 20 kHz; the low-frequency AAE (LAAE) was a 2–8 kHz band. The effects of sex, gonadectomy, and AAE treatment on genetic progressive hearing loss (a trait of B6 mice) were evaluated by obtaining auditory brainstem response (ABR) thresholds at ages 3-, 6-, and 9-months. At 9-months of age, hair cell counts (cytocochleograms) were obtained, and morphometric measures of the anteroventral cochlear nucleus (AVCN) were obtained. LAAE treatment caused elevation in ABR thresholds (8–24 kHz), with the highest thresholds occurring in intact females. LAAE treatment caused some loss of outer hair cells in the basal half of the cochlea (in addition to losses normally occurring in B6 mice), with intact females losing more cells than intact males. The loss of AVCN neurons and shrinkage of tissue volume that typically occur in 9-month-old B6 mice was lessened by LAAE treatment in intact (but not gonadectomized) male mice, whereas the degenerative changes were exacerbated in intact (but not gonadectomized) females. These LAAE effects were prominent in, but not restricted to, the tonotopic low-frequency (ventral) AVCN. HAAE treatment resulted in some loss of neurons in the high-frequency (dorsal) AVCN. In general, LAAE treatment plus male gonadal hormones (intact males) had an ameliorative effect whereas HAAE or LAAE treatment plus ovarian hormones (intact females) had a negative effect on age-related changes in the B6 auditory system.

Migration of neural precursor cells derived from olfactory bulb in cochlear nucleus exposed to an augmented acoustic environment

The regeneration of the auditory neural system remains a challenge in hearing restoration. Acoustic signals may induce a site-specific cell replacement in the auditory system. This hypothesis was tested with grafted implantation of neural precursor cells (NPCs) along the cochlear nucleus in the adult host followed by an augmented acoustic stimulation. NPCs were obtained from the olfactory bulbs at embryonic day 14–16 and were transplanted into the inside border of cochlear nucleus. The labeled cells survived at least 2 weeks, verified by Hoechst 33342 fluorescence, and by immunostaining for a neuronal marker. In some cases NPCs had migrated directionally to the root of the auditory nerve. This observation demonstrates the survival and migration of NPCs from the olfactory bulb (OB) along the adult auditory nerve in an augmented acoustic environment following implantation.

Effects of exposing gonadectomized and intact C57BL/6J mice to a high-frequency augmented acoustic environment: Auditory brainstem response thresholds and cytocochleograms

Gonadectomized and surgically intact adult C57BL/6J (B6) mice of both sexes were exposed for 12 h nightly to a high-frequency augmented acoustic environment (AAE): repetitive bursts of a half-octave noise band centered at 20 kHz, 70 dB SPL. The effects of sex, gonadectomy, and AAE treatment on genetic progressive hearing loss (exhibited by B6 mice) were evaluated by obtaining auditory brainstem response thresholds at ages 3-, 6-, and 9-months; hair cell counts (cytocochleograms) were obtained at 9 months. A sex difference in the rate of genetic progressive hearing loss in B6 mice (observed by earlier studies) was confirmed, with females exhibiting a faster rate of threshold elevations and more severe loss of hair cells at age 9 months. Gonadectomy had no consistent effects on the rate or severity of hearing loss in non-exposed mice of either sex. An unexpected finding was that the high-frequency AAE treatment caused additional ABR threshold elevations and hair cell loss. In an earlier study, the same high-frequency AAE treatment on DBA/2J mice ameliorated hearing loss. The most severe AAE-induced losses occurred in surgically intact females, suggesting a potentiating effect of ovarian hormone(s).

Effects of exposing DBA/2J mice to a high-frequency augmented acoustic environment on the cochlea and anteroventral cochlear nucleus

DBA/2J (D2) mice, which exhibit very early progressive sensorineural hearing loss, were treated for 12 h nightly with an augmented acoustic environment (AAE) initiated before the onset of hearing. The AAE consisted of repetitive bursts of a 70 dB sound pressure level, half-octave noise band centered at 20 kHz (i.e. low frequencies were excluded). At 55 days of age, AAE-treated mice, compared to control mice, exhibited less elevation of auditory brainstem response thresholds for tone frequencies from 16 to 32 kHz and fewer missing outer hair cells in the high-frequency tonotopic region of the cochlea. The dorsal region of their anteroventral cochlear nucleus (most strongly stimulated by the AAE) was larger, had more surviving neurons, and larger neurons than those of untreated control mice. These and previous findings using an AAE band containing lower frequencies indicate that AAE treatment effects are frequency-related. The findings provide support for the hypothesis that the beneficial effects of AAE treatment on the cochlea are associated with increased physiological activity evoked by the AAE, and the central AAE effects result from increased AAE-evoked neural activity and a healthier cochlea providing the auditory input.

Ameliorative Effects of Exposing DBA/2J Mice to an Augmented Acoustic Environment on Histological Changes in the Cochlea and Anteroventral Cochlear Nucleus

DBA/2J (D2) mice, which exhibit very early progressive sensorineural hearing loss, were treated nightly with an augmented acoustic environment (AAE) initiated before the onset of hearing, and consisting of repetitive bursts of a 70-dB sound pressure level (SPL), 4-25 kHz noise band. At 55 days of age, AAE-treated mice exhibited less elevation of auditory brainstem response thresholds, fewer missing hair cells, and greatly reduced loss of anteroventral cochlear nucleus (AVCN) volume and neuron number compared to untreated control mice. It was hypothesized that the central neuroprotective effect was associated with increased afferent input to AVCN neurons evoked by the AAE as well as a healthier cochlea.

Neural plasticity in the mouse inferior colliculus: relationship to hearing loss, augmented acoustic stimulation, and prepulse inhibition

C57BL/6J (C57) and DBA/2J (DBA) mice exhibit progressive high-frequency hearing loss. Extracellular recordings of responses of neurons in the inferior colliculus (IC) evoked by 70-dB SPL tones indicated that normal tonotopic organization was greatly disrupted in both strains: still-audible lower frequencies (4–12 kHz) evoked responses in a large percentage of recording sites in ventral tonotopic regions that normally respond strongly to high frequencies only. To relate the IC responses to an auditory behavior, prepulse inhibition (PPI) was measured using 70-dB tones as prepulses. As high-frequency hearing loss progressed in C57 mice, prepulses of 4–12 kHz elicited stronger PPI, and this was significantly correlated with changes in the percentage of IC recording sites responding to 70-dB tones (the neural pathway for PPI includes the IC). The analysis was extended to DBA mice that had been exposed to an augmented acoustic environment (AAE) – a procedure that improves PPI. In these mice, a higher percentage of IC recording sites responded to 70-dB tones, and this was correlated with improved PPI. The data suggest that responses of IC neurons reflect both hearing loss-induced plasticity and changes induced by exposure to an AAE, and these neural changes are correlated with the magnitude of PPI.

Progressive hearing loss in mouse models of presbycusis: Influence of an augmented acoustic environment and of gender

Progressive hearing loss associated with aging can be modulated by a number of genetic and environmental variables. Understanding how such variables work may suggest new approaches to ameliorate presbycusis. Two examples are long-term exposure to an augmented acoustic environment (AAE) and factors associated with gender (e.g., during the period of reproductive decline in females after 6 months of age). Research on inbred strains of mice that exhibit progressive hearing loss (C57BL/6J, BALB/cJ, DBA/2J) has demonstrated that daily exposure to a 70-dB SPL broadband noise AAE slows the progressive elevation of ABR thresholds, enhances behavioral responses to tones (startle response; prepulse inhibition), and affects histopathology of the cochlea and anteroventral cochlear nucleus (AVCN). However, gender plays a role in both the progression of hearing loss in nonexposed mice and the effects of the AAE. In the absence of AAE exposure, young C57BL/6J and BALB/cJ males and females have similar ABR thresholds, but hearing loss deteriorates more rapidly in females after around age 6 months. The auditory systems of males and females also respond differently to the AAE. Depending on gender, both positive and negative effects of AAE exposure are observed, although these effects are complicated.