Raphael, Y. Reorganization of the chick basilar papilla after acoustic trauma. J. Comp. Neurol. 330, 521−532

Kresge Hearing Research Institute, University of Michigan, Ann Arbor 48109-0506.
The Journal of Comparative Neurology (Impact Factor: 3.23). 04/1993; 330(4):521-32. DOI: 10.1002/cne.903300408
Source: PubMed


The auditory epithelium in birds and mammals consists of a postmitotic population of hair cells and supporting cells. Unlike mammals, birds can regenerate their auditory epithelia after trauma. Recent evidence indicates that supporting cells undergo mitosis after acoustic trauma, suggesting that supporting cells may transdifferentiate into hair cells. The goals of this study were to 1) characterize the responses of hair cells and supporting cells to acoustic trauma, and 2) determine whether hair cell loss is a prerequisite for generation of new hair cells. Chicks were exposed to an octave-band noise and their inner ears assayed with fluorescence or scanning electron microscopy. In one area of the basilar papilla, defined as the center of the lesion, extensive hair cell degeneration occurred. Expanded supporting cells obliterated degenerating hair cells and invaded spaces normally occupied by hair cells. Aggregates of DNA were found within the basilar papilla, suggesting that hair cell death and disintegration may occur within the epithelium. The epithelial sheet appeared structurally confluent at all times examined. Supporting cells exhibited altered apical contour in distal regions of the basilar papilla, where hair cell damage was mild or inconspicuous. Four days after noise exposure, newly generated hair cells were found in the center of the lesion and in the distal areas, where no hair cell loss could be detected. The results suggest that supporting cells may play an important role in maintenance and repair of the traumatized basilar papilla and raise the possibility that production of new hair cells is not dependent on hair cell loss in the immediate vicinity.

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    • "Two basic types of hair cell loss have been observed following acoustic injury. Investigators have noted that severely damaged hair cells may be ejected from the epithelium (Cotanche, 1987b; Cotanche et al., 1987; Cotanche and Dopyera, 1990) or disintegrate in situ (Raphael, 1993). In our study, it appears that hair cell ejection was a likely source of hair cell loss, given the presence of lesions in the saccular epithelium. "
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    ABSTRACT: Fishes are capable of regenerating sensory hair cells in the inner ear after acoustic trauma. However, a time course of auditory hair cell regeneration has not been established for zebrafish. Adult zebrafish (Danio rerio) were exposed to a 100 Hz pure tone at 179 dB re 1 microPa RMS for 36 h and then allowed to recover for 0-14 days before morphological analysis. Hair cell bundle loss and recovery were determined using phalloidin to visualize hair bundles. Cell proliferation was quantified through bromodeoxyuridine (BrdU) labeling. Immediately following sound exposure, zebrafish saccules exhibited significant hair bundle damage (e.g., splayed, broken, and missing stereocilia) and loss (i.e., missing bundles and lesions in the epithelia) in the caudal region. Hair bundle counts increased over the course of the experiment, reaching pre-treatment levels at 14 days post-sound exposure (dpse). Low levels of proliferation were observed in untreated controls, indicating that some cells of the zebrafish saccule are mitotically active in the absence of a damaging event. In sound-exposed fish, cell proliferation peaked two dpse in the caudal region, and to a lesser extent in the rostral region. This proliferation was followed by an increase in numbers of cuticular plates with rudimentary stereocilia and immature-like hair bundles at 7 and 14 dpse, suggesting that at least some of the saccular cell proliferation resulted in newly formed hair cells. This study establishes a time course of hair cell bundle regeneration in the zebrafish inner ear and demonstrates that cell proliferation is associated with the regenerative process.
    Full-text · Article · Apr 2009 · Hearing research
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    • "Conversely, new hair cells appear in the avian basilar papilla within four days after acoustic overstimulation or ototoxic treatment (Cotanche, 1987a; Cruz et al., 1987; Corwin and Cotanche, 1988; Ryals and Rubel , 1988; Raphael, 1992, 1993; Ryals et al., 1999; Dooling et al., 2006) and these cells become innervated and functional three days later (a total of seven days after insult; Wang and Raphael, 1996; Ofsie and Cotanche, 1996). The apical surfaces of surviving hair cells and supporting cells (Cotanche and Dopyera, 1990; Cotanche et al., 1991; Marsh et al., 1990; Raphael, 1993; Adler and Saunders, 1995) as well as dark cells in the tegmentum vasculosum (Ryals et al., 1995) return to near normal. The damaged tectorial membrane gains a new honeycombed pattern layer, at least partially restoring its shearing motion with the underlying hair cells in the region affected by noise (Cotanche, 1987b, 1992; Saunders et al., 1992; Adler et al., 1992, 1993, 1995a,b; Adler, 1996) or ototoxic drugs (Epstein and Cotanche, 1995). "
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    ABSTRACT: WD40 repeat 1 protein (WDR1) was first reported in the acoustically injured chicken inner ear, and bioinformatics revealed that WDR1 has numerous WD40 repeats, important for protein-protein interactions. It has significant homology to actin interacting protein 1 (Aip1) in several lower species such as yeast, roundworm, fruitfly and frog. Several studies have shown that Aip1 binds cofilin/actin depolymerizing factor, and that these interactions are pivotal for actin disassembly via actin filament severing and actin monomer capping. However, the role of WDR1 in auditory function has yet to be determined. WDR1 is typically restricted to hair cells of the normal avian basilar papilla, but is redistributed towards supporting cells after acoustic overstimulation, suggesting that WDR1 may be involved in inner ear response to noise stress. One aim of the present study was to resolve the question as to whether stress factors, other than intense sound, could induce changes in WDR1 presence in the affected avian inner ear. Several techniques were used to assess WDR1 presence in the inner ears of songbird strains, including Belgian Waterslager (BW) canary, an avian strain with degenerative hearing loss thought to have a genetic basis. Reverse transcription, followed by polymerase chain reactions with WDR1-specific primers, confirmed WDR1 presence in the basilar papillae of adult BW, non-BW canaries, and zebra finches. Confocal microscopy examinations, following immunocytochemistry with anti-WDR1 antibody, localized WDR1 to the hair cell cytoplasm along the avian sensory epithelium. In addition, little, if any, staining by anti-WDR1 antibody was observed among supporting cells in the chicken or songbird ear. The present observations confirm and extend the early findings of WDR1 localization in hair cells, but not in supporting cells, in the normal avian basilar papilla. However, unlike supporting cells in the acoustically damaged chicken basilar papilla, the inner ear of the BW canary showed little, if any, WDR1 up-regulation in supporting cells. This may be due to the fact that the BW canary already has established hearing loss and/or to the possibility that the mechanism(s) involved in BW hearing loss may not be related to WDR1.
    Full-text · Article · Jul 2008 · Hearing Research
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    • "The moderate noise level used in this study (118 dB SPL at 1.5 kHz for 5– 6 hours) induced partial hair cell damage and supporting cell expansion. In a moderately damaged basilar papilla (115–117 dB for 4 – 6 hours), the apical surfaces of the hair cells constrict, and the surrounding supporting cells expand their apical surfaces to maintain the continuity of the epithelial surface (Raphael, 1993; Cotanche et al., 1995). In comparison, a severe acoustic trauma with massive hair cell loss precluded complete Fig. 5 "
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    ABSTRACT: Auditory hair cells of birds, unlike hair cells in the mammalian organ of Corti, can regenerate following sound-induced loss. We have identified several genes that are upregulated following such an insult. One gene, WDR1, encodes the vertebrate homologue of actin-interacting protein 1, which interacts with actin depolymerization factor (ADF) to enhance the rate of actin filament cleavage. We examined WDR1 expression in the developing, mature, and noise-damaged chick cochlea by in situ hybridization and immunocytochemistry. In the mature cochlea, WDR1 mRNA was detected in hair cells, homogene cells, and cuboidal cells, all of which contain high levels of F-actin. In the developing inner ear, WDR1 mRNA was detected in homogene cells and cuboidal cells by embryonic day 7, in the undifferentiated sensory epithelium by day 9, and in hair cells at embryonic day 16. We also demonstrated colocalization of WDR1, ADF, and F-actin in all three cell types in the normal and noise-damaged cochlea. Immediately after acoustic overstimulation, WDR1 mRNA was seen in supporting cells. These cells contribute to the structural integrity of the basilar papilla, the maintenance of the ionic barrier at the reticular lamina, and the generation of new hair cells. These results indicate that one of the immediate responses of the supporting cell after noise exposure is to induce WDR1 gene expression and thus to increase the rate of actin filament turnover. These results suggest that WDR1 may play a role either in restoring cytoskeletal integrity in supporting cells or in a cell signaling pathway required for regeneration.
    Full-text · Article · Jul 2002 · The Journal of Comparative Neurology
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