Abstract
Tinnitus is an auditory phantom percept without external sound sources. Despite the high prevalence and tinnitus-associated distress of affected patients, the pathophysiology of tinnitus remains largely unknown, making prevention and treatments difficult to develop. In order to elucidate the pathophysiology of tinnitus, animal models are used where tinnitus is induced either permanently by noise trauma or transiently by the application of salicylate. In a model of trauma-induced tinnitus, we have suggested a central origin of tinnitus-related development of neuronal hyperactivity based on stochastic resonance (SR). SR refers to the physiological phenomenon that weak subthreshold signals for given sensors (or synapses) can still be detected and transmitted if appropriate noise is added to the input of the sensor. The main objective of this study was to characterize the neurophysiological and behavioral effects during salicylate-induced tinnitus and compare these to the conditions within the trauma model. Our data show, in line with the pharmacokinetics, that hearing thresholds generally increase 2 h after salicylate injections. This increase was significantly stronger within the region of best hearing compared to other frequencies. Furthermore, animals showed behavioral signs of tinnitus during that time window and frequency range as assessed by gap prepulse inhibition of the acoustic startle reflex (GPIAS). In contrast to animals with noise trauma-induced tinnitus, salicylate-induced tinnitus animals showed no correlation between hearing thresholds and behavioral signs of tinnitus, indicating that the development of tinnitus after salicylate injection is not based on SR as proposed for the trauma model. In other words, salicylate-induced tinnitus and noise trauma-induced tinnitus are not based on the same neurophysiological mechanism.
Highlights
Diseases of the inner ear that lead to hearing loss (HL) may result in subjective tinnitus (Ahlf et al, 2012), an auditory phantom sensation that is experienced, no physical sound is present
Once it was certain that the effect had disappeared, we proceeded with a second injection of either salicylate or saline in the same animals and obtained the GPIAS again to assess a possible acute tinnitus percept
We aimed to investigate the neurophysiological mechanisms underlying salicylate and trauma-induced tinnitus
Summary
Diseases of the inner ear that lead to hearing loss (HL) may result in subjective tinnitus (Ahlf et al, 2012), an auditory phantom sensation that is experienced, no physical sound is present. Several tinnitus models are being debated, due to developments in basic neuroscience, a central origin of tinnitusrelated activity seems to have replaced the former peripheral hypothesis (Noreña and Farley, 2013). Three main models, which are based on altered lateral inhibition, homeostatic plasticity, or stochastic resonance (SR) (Gerken, 1996; Eggermont and Roberts, 2004; Schaette and McAlpine, 2011; Ahlf et al, 2012; Tziridis et al, 2015; Leaver et al, 2016; Vanneste and De Ridder, 2016; Schilling et al, 2020), propose a central origin of tinnitus, resulting from damage to the cochlea as the initial step in tinnitus development
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