A novel technique for inducing local inner ear damage

Nakagawa, Takayuki; Kim, Tae Soo; Murai, Norihiko; Endo, Tamao; Iguchi, Fukuichiro; Tateya, Ichiro; Yamamoto, Norio; Naito, Yasushi; Ito, Juichi

doi:10.1016/s0378-5955(02)00768-2

Cited by 49 publications

(35 citation statements)

References 10 publications

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“…This expression has been observed in hair cells Ladrech et al, 2004;Mangiardi et al, 2004;Yang et al, 2004b;Hu et al, 2006), spiral ganglion cells (Ladrech et al, 2004;Labbe et al, 2005;Lang et al, 2005), stria vascularis and spiral ligament (Watanabe et al, 2003), and lateral wall (Labbe et al, 2005). Confirming an important role for caspase activation in the pathway to cell death, caspase inhibitors have been shown to prevent cell death in the inner ear after aminoglycoside treatment, chemotherapeutics, hypoxia, or NTF withdrawal (Cheng et al, 1999;Nakagawa et al, 2003;Zhang et al, 2003;Corbacella et al, 2004;Okuda et al, 2005;Wei et al, 2005).…”

Section: Caspase-dependent Cell Death: Extrinsic (Receptor-mediated) mentioning

confidence: 84%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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Recent research has shown the essential role of reduced blood flow and free radical formation in the cochlea in noise-induced hearing loss (NIHL). The amount, distribution, and time course of free radical formation have been defined, including a clinically significant late formation 7-10 days following noise exposure, and one mechanism underlying noise-induced reduction in cochlear blood flow has finally been identified. These new insights have led to the formulation of new hypotheses regarding the molecular mechanisms of NIHL; and, from these, we have identified interventions that prevent NIHL, even with treatment onset delayed up to 3 days post-noise. It is essential to now assess the additive effects of agents intervening at different points in the cell death pathway to optimize treatment efficacy. Finding safe and effective interventions that attenuate NIHL will provide a compelling scientific rationale to justify human trials to eliminate this single major cause of acquired hearing loss.

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Section: Caspase-dependent Cell Death: Extrinsic (Receptor-mediated) mentioning

confidence: 84%

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

et al. 2007

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“…Hair cell death due to aminoglycoside ototoxicity has been considered largely an apoptotic process and was not expected to be accompanied by an inflammatory response; thus, the abundance of cochlear inflammatory cells after kanamycin was not anticipated (Matsui et al 2003;Nakagawa et al 2003;Lee et al 2004;Tabuchi et al 2007;Goodyear et al 2008;Oesterle et al 2008;Taleb et al 2008;Taylor et al 2008). In this paper, we question whether the presence of inflammatory cells results in exacerbation of ototoxic injury or if they play a neutral role in phagocytosis of degenerated cells or even a beneficial role in repair of the sensory epithelium.…”

Section: Discussionmentioning

confidence: 99%

Expression of Fractalkine Receptor CX3CR1 on Cochlear Macrophages Influences Survival of Hair Cells Following Ototoxic Injury

Sato

Shick

Ransohoff

et al. 2009

JARO

112

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The role of innate immunity and macrophage recruitment to the inner ear after hair cell injury is a subject where little is known. In this paper, we demonstrate recruitment of monocytes and macrophages to the inner ear after kanamycin. We also examined the effect of fractalkine receptor (CX3CR1) deletion in kanamycin ototoxicity. We observed more functional and structural damage in CX3CR1 null mice compared to wild-type and heterozygous littermates. In order to determine if increased susceptibility to kanamycin resulted from CX3CR1 deletion from cochlear leukocytes, we created bone marrow chimeras by transplanting CX3CR1-null bone marrow into wild-type mice whose native bone marrow was ablated by lethal irradiation. These mice were then treated with kanamycin sulfate. Auditory brainstem responses (ABR), hair cell counts, and numbers of macrophages recruited to the cochlea were recorded in irradiated mice that received either wild-type, CX3CR1 heterozygous, or CX3CR1 knockout bone marrow. A strong correlation was present between numbers of macrophages and hair cell death in recipients transplanted with CX3CR1 null marrow. No correlation between macrophage number and hair cell loss was present in mice transplanted with wild-type or CX3CR1 heterozygous marrow. We suggest that CX3CR1 plays a role in modulating the detrimental effects of cochlear macrophages after kanamycin ototoxicity. Our data point to the possibility that CX3CR1-deficient cochlear macrophages exacerbate kanamycin ototoxicity while CX3CR1-expressing monocytes do not.

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“…Inconvenience of systemic administration: mortality caused by aminoglycoside-induced nephrotoxicity, associated with the high doses of antibiotics that are required to obtain sufficient hair cell damage, has already been observed in fish (Yan et al, 1991;Lombarte et al, 1993) as well as in the mouse (Nakagawa et al, 2003). In addition, previous studies demonstrated that in the oscar fish, intramuscular injection of gentamicin led to no apparent effect on saccular hair cells (Yan et al, 1991;Lombarte et al, 1993).…”

Section: Discussionmentioning

confidence: 99%

Effects of systemic versus local gentamicin on the inner ear in the Atlantic cod, Gadus morhua (L.), relevance for fish hearing investigations

et al. 2008

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a b s t r a c tFish models are increasingly being used for hearing research investigations. Aminoglycoside antibiotics that are used for damaging the inner ear hair cells can have systemic side effects leading to death of study animals. This study aimed to compare two methods: (i) systemic (intravenous) and (ii) local (intrasaccular) gentamicin administration for induction of inner ear hair cell damage in the Atlantic cod, Gadus morhua (L.). Hair cell damage was assessed using scanning electron microscopy; hair cell density, prevalence of immature hair cells and kinocilia length were measured. Gentamicin-treated fish were compared with control and sham fish. Intravenous gentamicin led to dose-dependent mortality caused by nephrotoxicity. The only visible effect after treatment was more immature hair cells and shorter kinocilia, the effect on hair cell density was equivocal. Following intrasaccular gentamicin treatment, fish mortality was negligible, and hair cells were damaged regardless of dose. Here, we observed decreased hair cell density, high prevalence of immature hair cells, and significantly shortened kinocilia. Conclusion: intrasaccular injection is preferable to intravenous injection of gentamicin for the study of ototoxicity in the Atlantic cod.

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A novel technique for inducing local inner ear damage

Cited by 49 publications

References 10 publications

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

Mechanisms of noise-induced hearing loss indicate multiple methods of prevention

Expression of Fractalkine Receptor CX3CR1 on Cochlear Macrophages Influences Survival of Hair Cells Following Ototoxic Injury

Effects of systemic versus local gentamicin on the inner ear in the Atlantic cod, Gadus morhua (L.), relevance for fish hearing investigations

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