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Nonconventional Clinical Applications of Otoacoustic Emissions: From Middle Ear Transfer to Cochlear Homeostasis to Access to Cerebrospinal Fluid Pressure
Published in Stavros Hatzopoulos, Andrea Ciorba, Mark Krumm, Advances in Audiology and Hearing Science, 2020
Blandine Lourenço, Fabrice Giraudet, Thierry Mom, Paul Avan
Given this generation mechanism, it is thus easily conceivable that DPOAEs exist in the absence of cochlear amplifier, provided OHCs still contain functional mechanotransduction channels in their hair bundles. This is indeed an unusual situation in which sensorineural hearing loss is due to too weak mechanotransduction currents when OHC transduction channels open (decreased endocochlear potential, for example, or impaired coupling between tectorial membrane and hair cells).
Anatomy of the Cochlea and Vestibular System: Relating Ultrastructure to Function
Published in John C Watkinson, Raymond W Clarke, Christopher P Aldren, Doris-Eva Bamiou, Raymond W Clarke, Richard M Irving, Haytham Kubba, Shakeel R Saeed, Paediatrics, The Ear, Skull Base, 2018
The fluid inside the lumen of the membranous canals is endolymph (Figure 47.1a). This has an unusual composition for an extracellular fluid. It is high in K+ (~140 mM) and low in Na+ (~1 mM). In the cochlea, endolymph also has a high positive electrical potential of around +80 mV, the endocochlear potential (EP), but although the compartments are interconnected a similar electrical potential is not observed in the vestibular system. The boundary between perilymph and endolymph lies at the level of the junctions between the epithelial cells that surround the endolymphatic spaces. These junctions form a permeability barrier, the maintenance of which is essential for the function of the inner ear.
Cochlear mechanisms and processes
Published in Stanley A. Gelfand, Hearing, 2017
Tasaki et al. (1954) measured a negative resting potential of about −60 to −70 mV in the organ of Corti, which is the intracellular potential (IP) of the hair cells (Dallos, 1973). Advances in measurement techniques enabled subsequent studies to provide a more accurate picture of the resting potentials of the inner and outer hair cells (Russell and Sellick, 1978a, 1983; Dallos et al., 1982; Dallos, 1985, 1986; Wangemann and Schacht, 1996). For example, Dallos and colleagues measured the electrical potentials in the upper turns of the guinea pig cochlea using a precisely controlled microelectrode that was advanced across the organ of Corti below and parallel to the reticular lamina (Dallos et al., 1982; Dallos, 1985, 1986). This approach enabled them to establish accurately intracellular potentials for both inner and outer hair cells, as well as to describe the details of both AC and DC intracellular receptor potentials, addressed below. Based on their data, it would appear that representative values are approximately −40 mV for the IHCs (as in Figure 4.12) and −70 mV for the OHCs (Dallos, 1985, 1986). The net result of the positive endocochlear potential and negative intracellular potential is an electrical polarity difference of 120 mV or more across the reticular lamina.
Mild hearing loss in C57BL6/J mice after exposure to antiretroviral compounds during gestation and nursing
Published in International Journal of Audiology, 2023
J. Riley DeBacker, Bo Hua Hu, Eric C. Bielefeld
The final measurement explored in the study was counting of OHCs and IHCs in a subset of ARV mice in order to determine underlying pathology associated with the threshold shift. Very few missing OHCs and IHCs were detected in the ARV mice. Therefore, it was concluded that OHC/IHC death was not the underlying pathology to explain the elevated thresholds. That said, there are several pathologies that can cause dysfunction of the hair cells, even if the cell itself is physically present. Stereocilia injury can prevent K+ ions from flowing into the hair cells, thus impairing their ability to undergo depolarisation and elevating auditory thresholds (Patuzzi 2002; Saunders and Flock 1986). OHCs without prestin are physically intact, but unable to provide cochlear amplification through electromotility (Liberman et al. 2002). Further, the depolarisation process of the hair cells is driven by the strong endocochlear potential in the endolymph, in which the approximately +80 mV positive charge creates a significant electrical gradient with the negative charge inside the hair cells. The endocochlear potential is generated by the active ion pumping from the marginal cells of the stria vascularis, and reduction of the endocochlear potential leads to elevated auditory thresholds (Mills and Schmiedt 2004). None of the aforementioned pathologies were visible with the assays employed in the current study. Therefore, none can be ruled out as possible contributors to the elevated ABR thresholds detected in the ARV mouse offspring group.
Vestibular suppression of normal bodily sounds
Published in Acta Oto-Laryngologica, 2020
Neil S. Longridge, Anielle Lim, Arthur Ian Mallinson, Jim Renshaw
The MOCS has also been observed during measurement of the basilar membrane motion and auditory activity of nerve fibers [6]. At high-intensity levels, the MOCS seems to influence basilar membrane responses by somehow increasing its stiffness [6]. MOCS activation can also reduce the endocochlear potential and as a result, cause a decrease in OHC and IHC output [6]. The activation of MOC increases the current flow through the OHCs which reduces the endocochlear potential through the dampening of the endocochlear potential battery [6]. The reduction in endocochlear potential also lowers the potential within the IHCs, which in turn decreases the overall activation of auditory nerve fibers [6]. MOC activation can also have an effect on the firing rates of auditory nerve fibers. The reduction in the endocochlear potential has the greatest effect on low-spontaneous and medium-spontaneous fibers which code for high-level sounds. Activation of MOC reduces the firing rate of those low- and medium-spontaneous fibers [6].
Temporal processing, spectral processing, and speech perception in noise abilities among individuals with chronic kidney disease undergoing hemodialysis
Published in Acta Oto-Laryngologica, 2021
Kaushlendra Kumar, Livingston Sengolraj, Mohan Kumar Kalaiah
Several investigations have reported a higher incidence of hearing loss among individuals with chronic kidney disease [1,2]. Hearing loss among these individuals has been attributed to the toxic effects of high blood urea, metabolic changes in the inner ear, and the use of ototoxic drugs [16]. Results of the present study showed poorer temporal processing, spectral processing, and speech perception in noise abilities among individuals with chronic kidney disease. Studies have shown that speech perception abilities are related to auditory processing abilities [12]. Thus, the poorer speech perception ability among individuals with chronic kidney disease could be a consequence of poorer temporal and spectral processing abilities. The auditory processing deficits observed in the present study are not unique to individuals with chronic kidney disease. Many investigations have documented poorer auditory processing among elderly adults compared to young adults [12,14,17]. Among elderly adults, the poorer auditory processing has been attributed to metabolic changes in the inner ear [17]. The poorer temporal and spectral processing abilities observed in the present study among individuals with chronic kidney disease could be a consequence of metabolic changes in the auditory system. Metabolic changes in the cochlea affect the functioning of stria vascularis, which is important for the maintenance of endocochlear potential in the inner ear, leading to hearing loss [18]. However, there is a lack of evidence to suggest that changes in endocochlear potential (or metabolic activity) affect auditory processing abilities without affecting hearing sensitivity.