Dynorphin release by the lateral olivocochlear efferents may inhibit auditory nerve activity: A cochlear drug delivery study

Prell, Colleen G. Le; Hughes, Larry F.; Bledsoe, Sanford C.

doi:10.1016/j.neulet.2014.04.024

Cited by 17 publications

(10 citation statements)

References 40 publications

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“…below). Furthermore, and in support of our hypothesis it has been shown that the lateral olivocochlear bundle could provide the required noise input to the AN, as disruption of lateral olivocochlear neurons with a dopaminergic neurotoxin depressed spontaneous auditory nerve activity (Le Prell et al, 2014) and efferent synapses of the lateral olivocochlear bundle re-innervate IHCs of the aged cochlea (Lauer et al, 2012). …”

Section: Discussionsupporting

confidence: 80%

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

et al. 2016

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Subjective tinnitus is generally assumed to be a consequence of hearing loss. In animal studies it has been demonstrated that acoustic trauma induced cochlear damage can lead to behavioral signs of tinnitus. In addition it was shown that noise trauma may lead to deafferentation of cochlear inner hair cells (IHC) even in the absence of elevated hearing thresholds, and it seems conceivable that such hidden hearing loss may be sufficient to cause tinnitus. Numerous studies have indicated that tinnitus is correlated with pathologically increased spontaneous firing rates and hyperactivity of neurons along the auditory pathway. It has been proposed that this hyperactivity is the consequence of a mechanism aiming to compensate for reduced input to the auditory system by increasing central neuronal gain, a mechanism referred to as homeostatic plasticity (HP), thereby maintaining mean firing rates over longer timescales for stabilization of neuronal processing. Here we propose an alternative, new interpretation of tinnitus-related development of neuronal hyperactivity in terms of information theory. In particular, we suggest that stochastic resonance (SR) plays a key role in both short- and long-term plasticity within the auditory system and that SR is the primary cause of neuronal hyperactivity and tinnitus. We argue that following hearing loss, SR serves to lift signals above the increased neuronal thresholds, thereby partly compensating for the hearing loss. In our model, the increased amount of internal noise—which is crucial for SR to work—corresponds to neuronal hyperactivity which subsequently causes neuronal plasticity along the auditory pathway and finally may lead to the development of a phantom percept, i.e., subjective tinnitus. We demonstrate the plausibility of our hypothesis using a computational model and provide exemplary findings in human patients that are consistent with that model. Finally we discuss the observed asymmetry in human tinnitus pitch distribution as a consequence of asymmetry of the distribution of auditory nerve type I fibers along the cochlea in the context of our model.

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Section: Discussionsupporting

confidence: 80%

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

et al. 2016

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“…As the stimulus level decreased, the derived estimates of f Tr linearized and the slope steeped at 0 Pa (or the operating point). Ouabain applied to the round window markedly reduced neural excitation in the basal half of the cochlear spiral, consistent with the idea that solutions applied to the cochlear base are limited to treating only the basal half of the cochlear spiral (Salt and Ma, 2001;Chen et al, 2005;Le Prell et al, 2014), increasing the magnitude but not the general sigmoidal saturating morphology of derived f Tr estimates.…”

Section: A Harmonic Analysis Applied To Cochlear Responsessupporting

confidence: 77%

An analysis of cochlear response harmonics: Contribution of neural excitation

Chertoff

Kamerer

Peppi

et al. 2015

The Journal of the Acoustical Society of America

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In this report an analysis of cochlear response harmonics is developed to derive a mathematical function to estimate the gross mechanics involved in the in vivo transfer of acoustic sound into neural excitation (f Tr ). In a simulation it is shown that the harmonic distortion from a nonlinear system can be used to estimate the nonlinearity, supporting the next phase of the experiment: Applying the harmonic analysis to physiologic measurements to derive estimates of the unknown, in vivo f Tr . From gerbil ears, estimates of f Tr were derived from cochlear response measurements made with an electrode at the round window niche from 85 Hz tone bursts. Estimates of f Tr before and after inducing auditory neuropathy-loss of auditory nerve responses with preserved hair cell responses from neurotoxic treatment with ouabain-showed that the neural excitation from low-frequency tones contributes to the magnitude of f Tr but not the sigmoidal, saturating, nonlinear morphology.

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“…In addition to classical neurotransmitters, dynorphin may modulate the neural output of the cochlea as the CAP amplitude is depressed following diffusion of the kappa-opioid receptor agonist (−) pentazocine across the round window membrane (Le Prell et al 2014). Finally, CGRP application increases the spike rate and decreases the mechanically driven response of primary afferents in the lateral line (Bailey and Fig.…”

Section: Control Of Auditory Nerve Fiber Excitability In the Adult Comentioning

confidence: 99%

Cochlear efferents in developing adult and pathological conditions

2015

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Cochlear activity is regulated by the olivo-cochlear bundle, which originates from the brainstem and projects onto the hair cells and auditory nerve fibers. Two efferent components can be distinguished: the medial and lateral olivo-cochlear efferent originating from the medial, and the lateral nuclei of the superior olivary complex. The input of the efferent systems on hair cells occurs during development and persists in the adult cochlea. Recent studies have shown that the efferent innervations are required to set the activity pattern in developing hair cells and auditory nerve fibers and to protect the synaptic structures in adult cochlea. In addition, efferent innervations undergo plasticity during pathological conditions such as noise-trauma or aging. This review discusses the mechanisms underlying the control of the hair cells and afferent fibers excitability by efferent neurons and their putative role in developing adult and pathological conditions.

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Dynorphin release by the lateral olivocochlear efferents may inhibit auditory nerve activity: A cochlear drug delivery study

Cited by 17 publications

References 40 publications

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

Stochastic Resonance Controlled Upregulation of Internal Noise after Hearing Loss as a Putative Cause of Tinnitus-Related Neuronal Hyperactivity

An analysis of cochlear response harmonics: Contribution of neural excitation

Cochlear efferents in developing adult and pathological conditions

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