Behavioral evaluation of auditory function abnormalities in adult rats with normal hearing thresholds that were exposed to noise during early development.

Noise-exposed rat pups provide a model of early deprivation of sensory input to the central auditory system, allowing the study of developmental neuroplasticity. Our previous results have demonstrated that a brief exposure of rats to broadband noise (125 dB SPL 8 min, 14th postnatal day) at the onset of hearing resulted in an altered intensity perception and frequency discrimination in adulthood despite normal hearing thresholds. In this study, we assessed the gap-detection ability and possible presence of tinnitus- and hyperacusis-like behavior in adult rats after the same neonatal acoustic trauma, using measurements of the acoustic startle response (ASR) in quiet and noisy environments and its prepulse inhibition by gaps in noise (gap-PPI). A significant deficit in the ability to detect gap was observed in the exposed rats when 55 dB SPL broadband noise was used as background. An increase of noise intensity to 65-75 dB SPL led to strengthening of the gap-PPI in exposed animals, which approached the gap-PPI values of control animals at these levels. Behavioral signs of tinnitus (gap detection deficits in 10 kHz narrow band noise) were found in 25% of exposed rats. An increased sensitivity to continuous noise was manifested in all exposed rats by suppression of the ASR at significantly lower background noise levels than in the controls. This effect was particularly pronounced in rats with tinnitus-like behavior. Our results indicate that neonatal acoustic trauma, producing only a transient threshold shift, may produce permanent abnormalities in suprathreshold auditory functions and the development of tinnitus and hyperacusis-like behavior.

Rybalko N ，Mitrovic D ，Šuta D ，Bureš Z ，Popelář J ，Syka J ... -  《-》

Is noise-induced cochlear neuropathy key to the generation of hyperacusis or tinnitus?

Hickox AE ，Liberman MC 《-》

Behavioral evidence for possible simultaneous induction of hyperacusis and tinnitus following intense sound exposure.

Chen G ，Lee C ，Sandridge SA ，Butler HM ，Manzoor NF ，Kaltenbach JA ... -  《-》

Effects of noise exposure on development of tinnitus and hyperacusis: Prevalence rates 12 months after exposure in middle-aged rats.

Fischer Brown Norway (FBN) rats (n = 233) were unilaterally exposed to 12 different combinations of noise intensity, duration, and spectrum, while 46 rats served as sham-exposed controls. Rats were behaviorally tested for tinnitus and hyperacusis using gap-induced inhibition of the acoustic startle reflex (Gap) and prepulse inhibition (PPI) using 60-dB SPL before noise-exposure and at regular intervals for 12 mo. 12-mo after noise exposure the middle-aged rats were then tested again for tinnitus and hyperacusis before collecting Auditory Brainstem Response (ABR) thresholds. Collapsing across all noise exposure conditions a significant tinnitus-like deficit in responding to silent gaps was observed, with the most likely tinnitus pitch around 16 kHz. Rates of tinnitus 12-mo after noise exposure were greatest in groups receiving the four least intense noise doses (110-dB for 30, 60 and 120 min, and 116-dB for 30 min), while some of the greatest rates of hyperacusis occurred in groups receiving more intense or longer exposures. The results suggest that rates for developing tinnitus in animal models may not be easily predicted based upon noise exposure dose, but that low-to-moderate noise exposures may result in the greatest likelihood for producing tinnitus.

Turner JG ，Larsen D 《-》

Strain Comparison in Rats Differentiates Strain-Specific from More General Correlates of Noise-Induced Hearing Loss and Tinnitus.

Experiments in rodent animal models help to reveal the characteristics and underlying mechanisms of pathologies related to hearing loss such as tinnitus or hyperacusis. However, a reliable understanding is still lacking. Here, four different rat strains (Sprague Dawley, Wistar, Long Evans, and Lister Hooded) underwent comparative analysis of electrophysiological (auditory brainstem responses, ABRs) and behavioral measures after noise trauma induction to differentiate between strain-dependent trauma effects and more consistent changes across strains, such as frequency dependence or systematic temporal changes. Several hearing- and trauma-related characteristics were clearly strain-dependent. Lister Hooded rats had especially high hearing thresholds and were unable to detect a silent gap in continuous background noise but displayed the highest startle amplitudes. After noise exposure, ABR thresholds revealed a strain-dependent pattern of recovery. ABR waveforms varied in detail among rat strains, and the difference was most prominent at later peaks arising approximately 3.7 ms after stimulus onset. However, changes in ABR waveforms after trauma were small compared to consistent strain-dependent differences between individual waveform components. At the behavioral level, startle-based gap-prepulse inhibition (gap-PPI) was used to evaluate the occurrence and characteristics of tinnitus after noise exposure. A loss of gap-PPI was found in 33% of Wistar, 50% of Sprague Dawley, and 75% of Long Evans rats. Across strains, the most consistent characteristic was a frequency-specific pattern of the loss of gap-PPI, with the highest rates at approximately one octave above trauma. An additional range exhibiting loss of gap-PPI directly below trauma frequency was revealed in Sprague Dawley and Long Evans rats. Further research should focus on these frequency ranges when investigating the underlying mechanisms of tinnitus induction.

Koch L ，Gaese BH ，Nowotny M 《-》