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Unilateral auditory deprivation induces a reduction in the acoustic reflex threshold (ART) and an increase in loudness. These findings have been interpreted as a compensatory change in neural gain, governed by changes in excitatory and inhibitory neural inputs. There is also evidence to suggest that changes in neural gain can be measured using the auditory brainstem response (ABR). The present study extended Munro et al. (2014) [J. Acoust. Soc. Am. 135, 315-322] by investigating changes after 4 days of unilateral earplug use to: (i) ART, (ii) ABR and (iii) loudness. Because changes may occur during the post-deprivation test session (day 4), ART measurements were taken 1 h and 2 h post-earplug removal. There was a significant reduction in ART in the treatment ear immediately after the removal of the earplug, which is consistent with a compensatory increase in neural gain. A novel finding was the significant return of ARTs to baseline within 2 h of earplug removal. A second novel finding was a significant decrease in the mean amplitude of ABR wave V in the treatment ear, but a significant increase in the control ear, both after 4 days of deprivation. These changes in the ABR are in the opposite direction to those predicted. We were unable to replicate the change in loudness reported in previous deprivation studies; however, the short period of earplug use may have contributed to this null finding., (Copyright © 2017 Elsevier B.V. All rights reserved.)

The phantom auditory sensation of tinnitus is now studied in humans, animals, and computer models, and our understanding of how tinnitus is triggered and which neural mechanisms give rise to the phantom sensation in the brain has increased considerably. In most cases, tinnitus is associated with hearing loss, and even tinnitus patients with normal hearing thresholds might have cochlear damage that is not detected through conventional audiometry, as has been recently shown through auditory brainstem response measurements. Animals show behavioural signs of tinnitus after induction of hearing loss, indicating a causal relation. Moreover, surgical reduction of hearing loss in otosclerosis can reduce or even abolish tinnitus. However, hearing loss does not always lead to tinnitus. Psychophysical measurements have indicated that certain types of cochlear damage might be more closely linked to tinnitus than others. Recent animal studies have used behavioural testing to distinguish between animals with and without tinnitus after noise exposure. Comparisons between these groups of animals have helped identify neural correlates of tinnitus as well as factors that could represent a predisposition for tinnitus. Human neuroimaging studies have also begun to separate the neural signature of tinnitus from other consequences of hearing loss. The functional mechanisms that could underlie tinnitus development tinnitus have been analysed in computational modelling studies, which indicate that tinnitus could be a side-effect of the brain's attempt to compensate for hearing loss. Even though causal treatments for tinnitus are currently not available, hearing aids can provide considerable benefit when used in conjunction with counselling, tinnitus retraining therapy or cognitive behavioural therapy. Finally, animal studies demonstrate that the development of chronic noise-induced tinnitus might be prevented through timely interventions after noise exposure. This article is part of a Special Issue entitled ., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Auditory deprivation and stimulation can change the threshold of the acoustic middle ear reflex as well as loudness in adult listeners. However, it has remained unclear whether changes in these measures are due to the same mechanism. In this study, deprivation was achieved using a monaural earplug that was worn by listeners for 7 days. Acoustic reflex thresholds (ARTs) and categorical loudness ratings were measured using a blinded design in which the experimenter was unaware of which ear had been plugged. Immediately after terminating unilateral deprivation, ARTs were obtained at a lower sound pressure level in the ear that had been fitted with an earplug and at a higher sound pressure level in the control ear. In contrast, categorical judgments of loudness changed in the same direction in both ears with a given stimulus level reported as louder after unilateral deprivation. The relationship between changes to the ART and loudness judgments was not statistically significant. For both the ARTs and the categorical loudness judgments, most of the changes had disappeared within 24 h after earplug removal. The changes in ARTs, as a consequence of unilateral sound deprivation, are consistent with a gain control mechanism; however, the lack of relationship with the categorical loudness judgments, and the different pattern of findings for each measure, suggests the possibility of multiple gain mechanisms.

Cochlear damage can change the spontaneous firing rates of neurons in the dorsal cochlear nucleus (DCN). Increased spontaneous firing rates (hyperactivity) after acoustic trauma have been observed in the DCN of rodents such as hamsters, chinchillas and rats. This hyperactivity has been interpreted as a neural correlate of tinnitus. In cats, however, the spontaneous firing rates of DCN neurons were not significantly elevated after acoustic trauma. Species-specific spontaneous firing rates after cochlear damage might be attributable to differences in the response types of DCN neurons: In gerbils, type III response characteristics are predominant, whereas in cats type IV responses are more frequent. To address the question of how the development of hyperactivity after cochlear damage depends on the response type of DCN neurons, we use a computational model of the basic circuit of the DCN. By changing the strength of two types of inhibition, we can reproduce salient features of the responses of DCN neurons. Simulated cochlear damage, which decreases the activity of auditory nerve fibers, is assumed to activate homeostatic plasticity in projection neurons (PNs) of the DCN. We find that the resulting spontaneous firing rates depend on the response type of DCN PNs: PNs with type III and type IV-T response characteristics may become hyperactive, whereas type IV PNs do not develop increased spontaneous firing rates after acoustic trauma. This theoretical framework for the mechanisms and circumstances of the development of hyperactivity in central auditory neurons might also provide new insights into the development of tinnitus.

Tinnitus, the perception of a sound in the absence of acoustic stimulation, is often associated with hearing loss. Animal studies indicate that hearing loss through cochlear damage can lead to behavioral signs of tinnitus that are correlated with pathologically increased spontaneous firing rates, or hyperactivity, of neurons in the auditory pathway. Mechanisms that lead to the development of this hyperactivity, however, have remained unclear. We address this question by using a computational model of auditory nerve fibers and downstream auditory neurons. The key idea is that mean firing rates of these neurons are stabilized through a homeostatic plasticity mechanism. This homeostatic compensation can give rise to hyperactivity in the model neurons if the healthy ratio between mean and spontaneous firing rate of the auditory nerve is decreased, for example through a loss of outer hair cells or damage to hair cell stereocilia. Homeostasis can also amplify non-auditory inputs, which then contribute to hyperactivity. Our computational model predicts how appropriate additional acoustic stimulation can reverse the development of such hyperactivity, which could provide a new basis for treatment strategies.

Reliable accounts of the variability observed in neural spike trains are a prerequisite for the proper interpretation of neural dynamics and coding principles. Models that accurately describe neural variability over a wide range of stimulation and response patterns are therefore highly desirable, especially if they can explain this variability in terms of basic neural observables and parameters such as firing rate and refractory period. In this work, we analyze the response variability recorded in vivo from locust auditory receptor neurons under acoustic stimulation. In agreement with results from other systems, our data suggest that neural refractoriness has a strong influence on spike-train variability. We therefore explore a stochastic model of spike generation that includes refractoriness through a recovery function. Because our experimental data are consistent with a renewal process, the recovery function can be derived from a single interspike-interval histogram obtained under constant stimulation. The resulting description yields quantitatively accurate predictions of the response variability over the whole range of firing rates for constant-intensity as well as amplitude-modulated sound stimuli. Model parameters obtained from constant stimulation can be used to predict the variability in response to dynamic stimuli. These results demonstrate that key ingredients of the stochastic response dynamics of a sensory neuron are faithfully captured by a simple stochastic model framework.