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INNER EAR

Long-term administration of vasopressin can cause Ménière’s disease in mice

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Pages 990-1004 | Received 06 Mar 2014, Accepted 06 Mar 2014, Published online: 18 Aug 2014
 

Abstract

Conclusion: A new murine model of Ménière’s disease has been developed, based on long-term administration of vasopressin. Induction of vestibular dysfunction in the present animal model can cause additional stress, by reducing inner ear blood flow. Latanoprost, a selective agonist for the FP prostanoid receptor, may become a new remedy for Ménière’s disease. Objective: The purpose of this study was to develop a more suitable animal model, with a closer resemblance to the pathophysiological process in Ménière’s disease. Methods: Adult CBA/J or ICR mice were treated by subcutaneous injection of vasopressin for 5 days up to 8 weeks. Morphological analyses were performed of the cochlea, vestibular end organs and endolymphatic sac. The effect of latanoprost on the development of endolymphatic hydrops was also examined. Results: All experimental animals showed mild to moderate endolymphatic hydrops, increasing in severity as the vasopressin treatment was prolonged. Animals treated with vasopressin for 8 weeks showed severe endolymphatic hydrops with partial loss of outer hair cells and spiral ganglion cells. These animals also had a reversible vestibular dysfunction following intratympanic injection of epinephrine. Latanoprost inhibited the development of endolymphatic hydrops caused by vasopressin.

Acknowledgments

This study was supported by a Health and Labor Science Research Grant for Research on Specific Disease (Vestibular Disorders) from the Ministry of Health, Labor and Welfare, Japan (2013), a Grant-in-Aid for Scientific Research (25462643) provided by the Ministry of Education, Science and Culture, Japan and also by the Swedish Medical Research Council (grant no. 17X-7305 to M.A.).

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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