Abstract
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.
Highlights
In addition to increasing age, the strongest determinant for hearing loss is damage to the sensory cells within the cochlea caused by noise exposure (Liberman and Dodds 1984)
auditory brainstem response (ABR) hearing thresholds and acoustic startle responses were determined before noise exposure to provide a baseline comparison of the four different rat strains
The most consistent characteristic was a frequency-specific pattern of tinnitus prevalence, with the highest rates at approximately one octave above and below the center frequency of acoustic trauma found in Long Evans and Sprague Dawley rats
Summary
In addition to increasing age, the strongest determinant for hearing loss is damage to the sensory cells within the cochlea caused by noise exposure (Liberman and Dodds 1984). A malfunction of these peripheral structures leads to decreased transmission of auditory information to higher processing centers, thereby impairing hearing ability and leading to perceptual anomalies such as tinnitus, hyperacusis, or hidden hearing loss (Sheppard et al 2020). Noise-induced hearing loss often accompanies tinnitus (Eggermont and Roberts 2015). No reliable, effective therapy is available for tinnitus patients (Sheppard et al 2020), partially because the underlying pathological changes of tinnitus induction and persistence remain unclear. Among them are mice (Hickox and Liberman 2014; Liberman and Liberman 2015; Nowotny et al 2017; Park et al 2020), gerbils (Nowotny et al 2011; Kiefer et al 2015; Schilling et al 2017; Jeschke et al 2021), hamsters (Chen et al 2013; Manzoor et al 2013), guinea pigs (Mulders et al 2014; Hockley et al 2020), and rats (Turner et al 2006; Caspary et al 2008; Lobarinas et al 2013; Möhrle et al 2019; van Zwieten et al 2021)
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