Cochlear homeostasis: a molecular physiological perspective on maintenance of sound transduction and auditory neurotransmission with noise and ageing

Housley, Gary D.; Jonquières, Georg von; Pinyon, Jeremy L.; Matheson, Julie-Anne T.; Pearson, Lily J; Salthouse, Theresa P; Cederholm, Jennie M. E.

doi:10.1016/j.cophys.2020.09.012

Cited by 4 publications

(4 citation statements)

References 103 publications

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“…Reduction of OHC electro-mechanical transduction by the MOC efferent pathway is otoprotective ( 14 , 35 ). For example, surgical ablation of the COCB at the floor of the fourth ventricle in cats increased noise-induced threshold shifts ( 36 ) and over-expression of the OHC α9 nicotinic acetylcholine receptor subunit in mice confers protection to noise-induced hearing loss (NIHL) ( 37 ).…”

Section: Resultsmentioning

confidence: 99%

Noise-induced hearing loss vulnerability in type III intermediate filament peripherin gene knockout mice

et al. 2022

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In the post-natal mouse cochlea, type II spiral ganglion neurons (SGNs) innervating the electromotile outer hair cells (OHCs) of the ‘cochlear amplifier' selectively express the type III intermediate filament peripherin gene (Prph). Immunolabeling showed that Prph knockout (KO) mice exhibited disruption of this (outer spiral bundle) afferent innervation, while the radial fiber (type I SGN) innervation of the inner hair cells (~95% of the SGN population) was retained. Functionality of the medial olivocochlear (MOC) efferent innervation of the OHCs was confirmed in the PrphKO, based on suppression of distortion product otoacoustic emissions (DPOAEs) via direct electrical stimulation. However, “contralateral suppression” of the MOC reflex neural circuit, evident as a rapid reduction in cubic DPOAE when noise is presented to the opposite ear in wildtype mice, was substantially disrupted in the PrphKO. Auditory brainstem response (ABR) measurements demonstrated that hearing sensitivity (thresholds and growth-functions) were indistinguishable between wildtype and PrphKO mice. Despite this comparability in sound transduction and strength of the afferent signal to the central auditory pathways, high-intensity, broadband noise exposure (108 dB SPL, 1 h) produced permanent high frequency hearing loss (24–32 kHz) in PrphKO mice but not the wildtype mice, consistent with the attenuated contralateral suppression of the PrphKO. These data support the postulate that auditory neurons expressing Prph contribute to the sensory arm of the otoprotective MOC feedback circuit.

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Section: Resultsmentioning

confidence: 99%

Noise-induced hearing loss vulnerability in type III intermediate filament peripherin gene knockout mice

et al. 2022

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“…In the absence of TTS, the P2rx2 KO mice exhibited normal hearing sensitivity at a young age but developed accelerated age-related hearing loss compared to wildtype mice. In addition, P2rx2 KO mice demonstrated increased vulnerability to sustained loud sound at higher noise levels (95 dB SPL), developing significantly higher permanent threshold shifts (PTS) than wildtype mice [ 8 , 22 , 46 ].…”

Section: P2 Receptors In the Cochleamentioning

confidence: 99%

“…Several lines of evidence also support the notion that ATP-dependent mechanisms safeguard against the harmful effects of acoustic overstimulation in the adult cochlea [ 8 ]. Purinergic-mediated adaptation of the cochlear sensory structures to loud sound decreases the activity of the sensory cells and protects them and their afferent synapses from sustained noise exposure and acoustic injury [ 22 ].…”

Section: Introductionmentioning

confidence: 99%

Purinergic Signalling in the Cochlea

Vlajkovic

Thorne

2022

IJMS

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The mammalian cochlea is the sensory organ of hearing with a delicate, highly organised structure that supports unique operating mechanisms. ATP release from the secretory tissues of the cochlear lateral wall (stria vascularis) triggers numerous physiological responses by activating P2 receptors in sensory, supporting and neural tissues. Two families of P2 receptors, ATP-gated ion channels (P2X receptors) and G protein-coupled P2Y receptors, activate intracellular signalling pathways that regulate cochlear development, homeostasis, sensory transduction, auditory neurotransmission and response to stress. Of particular interest is a purinergic hearing adaptation, which reflects the critical role of the P2X2 receptor in adaptive cochlear response to elevated sound levels. Other P2 receptors are involved in the maturation of neural processes and frequency selectivity refinement in the developing cochlea. Extracellular ATP signalling is regulated by a family of surface-located enzymes collectively known as “ectonucleotidases” that hydrolyse ATP to adenosine. Adenosine is a constitutive cell metabolite with an established role in tissue protection and regeneration. The differential activation of A1 and A2A adenosine receptors defines the cochlear response to injury caused by oxidative stress, inflammation, and activation of apoptotic pathways. A1 receptor agonism, A2A receptor antagonism, and increasing adenosine levels in cochlear fluids all represent promising therapeutic tools for cochlear rescue from injury and prevention of hearing loss.

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“…Reduction of OHC electro-mechanical transduction by the MOC efferent pathway is otoprotective (Park et al, 2017, Housley et al, 2020. For example, surgical ablation of the COCB at the floor of the fourth ventricle in cats increased noise-induced threshold shifts (Rajan, 2000) and overexpression of the OHC α9 nicotinic acetylcholine receptor subunit in mice confers protection to NIHL (Maison et al, 2002).…”

Section: Loss Of Otoprotection From Noise-induced Hearing Loss In Prph Knockout Micementioning

confidence: 99%

Association of cochlear outer hair cell - type II spiral ganglion afferents with protection from noise-induced hearing loss

Cederholm

Parley

Perera

et al. 2021

Preprint

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The medial olivocochlear (MOC) efferent feedback circuit projecting to the cochlear outer hair cells (OHCs) confers protection from noise-induced hearing loss and is generally thought to be driven by inner hair cell (IHC) - type I spiral ganglion afferent (SGN) input. Knockout of the Prph gene (PrphKO) encoding the peripherin type III intermediate filament disrupted the OHC - type II SGN innervation and virtually eliminated MOC – mediated contralateral suppression from noise delivered to the opposite ear, measured as a reduction in cubic distortion product otoacoustic emissions. Electrical stimulation of the MOC pathway elicited contralateral suppression indistinguishable between wildtype (WT) and PrphKO mice, indicating that the loss of contralateral suppression was not due to disruption of the efferent arm of the circuit; IHC – type I SGN input was also normal, based on auditory brainstem responses. High-intensity, broadband noise (108 dB SPL, 1 hour) produced permanent hearing loss in PrphKO mice, but not in WT littermates. These findings associate OHC-type II input with MOC efferent - based otoprotection at loud sound levels.

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Cochlear homeostasis: a molecular physiological perspective on maintenance of sound transduction and auditory neurotransmission with noise and ageing

Cited by 4 publications

References 103 publications

Noise-induced hearing loss vulnerability in type III intermediate filament peripherin gene knockout mice

Noise-induced hearing loss vulnerability in type III intermediate filament peripherin gene knockout mice

Purinergic Signalling in the Cochlea

Association of cochlear outer hair cell - type II spiral ganglion afferents with protection from noise-induced hearing loss

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