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Ouabain-Induced Auditory Nerve Degeneration in Congenic ly5.1 Mice

Journal of Otology 2011年第2期6卷 19-28页

作者： Lauren A.Kilpatrick Devadoss J Samuvel ZHU Ju-hong Nancy Smythe LANG Hai-nan Department of Pathology and Laboratory Medicine Medical University of South Carolina Charleston SC 29425 United States Department of Otolaryngology - Heary & Neck Surgery Medical University of South Carolina Charleston SC 29425 United States

The ly5.1 mouse,also termed ***-Ptprca Pepcb/BoyJ,is a congenic strain widely used as a recipient in animal studies of bone marrow *** previous study documented that a majority of type I spiral ganglion neurons (SGNs) in the apical turns of ly5.1 mice are unmyelinated and aggregate into neuronal clusters,similar to the spiral ganglion in the human ***,a well known Na-K ATPase inhibitor,has been shown to induce neuronal degeneration in a variety of neural tissues including the adult gerbil and CBA/CaJ mouse spiral ***,functional and pathological changes of the auditory nerves in young-adult ly5.1 mice were examined at 3,7 and 14 days after ouabain *** to observations in CBA/CaJ mice,ouabain application selectively removed type I SGNs,resulting in an immense decline of the auditory nerve *** of glial cells was seen in the injured auditory nerves at 7 days after ouabain *** data indicate that the 'human-like' features of unmyelinated type I SGNs have no protective impact on the fate of SGNs after ouabain *** incorporating bromodeoxyuridine (BrdU) and expressing Sox2 were also counted in the auditory nerves of control and ouabain-treated *** number of Sox2+ glial cells significantly increased at 3 and 7 days ***,the highest density of BrdU+ cells appeared in the apical turn of the injured auditory nerve shortly after ouabain exposure,suggesting that the pattern of SGN loss at the apical turn in ly5.1 mouse may have some impact on the reaction of non-neuronal cells in response to acute ototoxic drug exposure in the auditory nerve.

关键词： primary auditory nerve ly5.1 mouse ouabain neural degeneration Sox2 BrdU glial cells

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