Blebs in inner and outer hair cells: a pathophysiological hypothesis

Ramírez‐Camacho, Rafael; García-Berrocal, José Ramón; Trinidad, Almudena; Verdaguer, José María; Nevado, Julián

doi:10.1017/s002221510700134x

Cited by 9 publications

(7 citation statements)

References 24 publications

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“…Similar findings have been previously noticed in cisplatin-treated guinea pigs [31] and following loud auditory stimulation [32]. Being noticed in relation to the IHC in an in vitro isolated organ of Corti of adult guinea pigs [33], these authors considered these blebs as physiological features arising as a result of an imbalance of endocytosis and exocytosis in the apical plasma membrane, linked to Na + loading which occurs in vitro [33].…”

Section: Discussionsupporting

confidence: 70%

“…Being noticed in relation to the IHC in an in vitro isolated organ of Corti of adult guinea pigs [33], these authors considered these blebs as physiological features arising as a result of an imbalance of endocytosis and exocytosis in the apical plasma membrane, linked to Na + loading which occurs in vitro [33]. On the other hand, they have been proposed to be an early degenerative change that develops when actin attachments between the plasma membrane of the hair cell and the underlying cytoskeleton were weakened [31]. Since these blebs were characteristically observed in this work following the use of high dose of nicotine they could be as an association with apoptotic hair cell injury as suggested by [34].…”

Section: Discussionmentioning

confidence: 99%

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Effect of nicotine on the structure of cochlea of guinea pigs

et al. 2014

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Smoking has been positively associated with hearing loss in human. However, its effect on the cochlea has not been previously evaluated. Aim of work is to investigate the effect of nicotine, which is the primary pharmacological component of tobacco, on the structure of the cochlea of adult male guinea pigs. Fifteen male guinea pigs were classified into two groups: group I (control) and group II (nicotine treated group). Group II was further subdivided into two subgroups; IIA and IIB according to the dose of nicotine (3 mg/kg and 6 mg/kg, respectively). The cochlea was harvested and processed for light microscopy, transmission electron microscopy and scanning electron microscopy. Nicotine administration induced damage of outer hair cells which were distorted in shape with vacuolated cytoplasm and heterochromatic nuclei. Topography revealed damage of the stereocilia which included disorganization, bent and limp or complete loss and expansion of the surrounding supporting cells. These changes were more pronounced in the basal turn of the cochlea and mainly involved the outer hair cells. High dose induced more damage and resulted in protrusion of the apical poles of hair cells (blebing), particularly the outer two rows. Nicotine is proved to be harmful to the cells of the cochlea, particularly the outer hair cells of the basal turn. High doses induce blebing of hair cells.

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Section: Discussionsupporting

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Effect of nicotine on the structure of cochlea of guinea pigs

et al. 2014

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“…This supports the idea that massive apical exocytosis occurred in the hair cells in order to evacuate an excess of metabolic waste that had accumulated in the cell body during the sound exposure. Alternatively, or additionally, blebbing could be a sign of the regulation of hair cell intracellular pressure, as suggested for cisplatin‐treated animals (Ramírez‐Camacho et al, ). Likely, both mechanisms, waste evacuation or pressure adjustment, would be expected to promote hair cell survival.…”

Section: Discussionmentioning

confidence: 92%

Cochlear neuropathy in the rat exposed for a long period to moderate‐intensity noises

Gannouni

Lenoir

Rhouma

et al. 2015

J of Neuroscience Research

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Damaging effects on the cochlea of high-intensity acoustic overexposures have been extensively documented, but only few works have focused on the danger of moderate noise levels. Using scanning and transmission electron microscopy, we explored the noise-induced neuroepithelial changes that occur in the cochlea of rats subjected to moderate intensities, 70 and 85 dB SPL, for an extended period of time (6 hr/day over 3 months). Although the full quota of outer and inner sensory hair cells remained present, we detected discrete abnormalities, likely resulting from metabolic impairment, in both types of hair cell within the basal region of the cochlea. In contrast, important noise-dependent losses of spiral ganglion neurons had occurred. In addition, we found cytoplasmic accumulations of lipofuscin-like aggregates in most of the surviving cochlear neurons. These results strongly suggest that noise levels comparable to those of certain working environments, with sufficient exposure duration, pose a severe risk to the cochlea. Moreover, our data support the notion that long-duration exposure to moderate noise is a causative factor of presbycusis.

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“…2 The ototoxic effects of cisplatin include loss of outer hair cells, blebbing of outer and inner hair cells, degeneration of the stria vascularis, and a decrease in the number of spiral ganglion cells. 5 In the kidney, cisplatin highly accumulates in cells of the terminal proximal tubule and of the distal nephron, where it causes either apoptosis or necrosis, depending on exposure time and concentration. 2 Recently, some attention has been paid to the role of specific cellular uptake processes in cisplatin toxicity.…”

mentioning

confidence: 99%

Organic Cation Transporter 2 Mediates Cisplatin-Induced Oto- and Nephrotoxicity and Is a Target for Protective Interventions

Ciarimboli

Deuster

Knief

et al. 2010

The American Journal of Pathology

389

341

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The use of the effective antineoplastic agent cisplatin is limited by its serious side effects , such as oto-and nephrotoxicity. Ototoxicity is a problem of special importance in children , because deafness hampers their language and psychosocial development. Recently , organic cation transporters (OCTs) were identified in vitro as cellular uptake mechanisms for cisplatin. In the present study , we investigated in an in vivo model the role of OCTs in the development of cisplatin oto-and nephrotoxicity. The functional effects of cisplatin treatment on kidney (24 hours excretion of glucose , water , and protein) and hearing (auditory brainstem response) were studied in wildtype and OCT1/2 double-knockout (KO) mice. No sign of ototoxicity and only mild nephrotoxicity were observed after cisplatin treatment of knockout mice. Comedication of wild-type mice with cisplatin and the organic cation cimetidine protected from ototoxicity and partly from nephrotoxicity. For the first time we showed that OCT2 is expressed in hair cells of the cochlea. Furthermore , cisplatin-sensitive cell lines from pediatric tumors showed no expression of mRNA for OCTs , indicating the feasibility of therapeutic approaches aimed to reduce cisplatin toxicities by competing OCT2-mediated cisplatin uptake in renal proximal tubular and cochlear hair cells. These findings are very important to establish chemotherapeutical protocols aimed to maximize the antineoplastic effect of cisplatin while reducing the risk of toxicities.

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Blebs in inner and outer hair cells: a pathophysiological hypothesis

Abstract: Cisplatin seems to be able to induce changes in inner hair cells as well as in other structures in the organ of Corti. Blebbing observed in animals following cisplatin administration could play a specific role in the regulation of intracellular pressure.

Cited by 9 publications

References 24 publications

Effect of nicotine on the structure of cochlea of guinea pigs

Effect of nicotine on the structure of cochlea of guinea pigs

Cochlear neuropathy in the rat exposed for a long period to moderate‐intensity noises

Organic Cation Transporter 2 Mediates Cisplatin-Induced Oto- and Nephrotoxicity and Is a Target for Protective Interventions

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