Abstract
In this paper the current state of knowledge of the development in experimental endolymphatic hydrops (EEH) is summarized, with particular emphasis on calcium. An imbalanced Ca2+ homeostasis in the inner ear is demonstrated using EEH as an animal model for Meniere's disease. The possibility of a receptor-mediated Ca2+ transport across the epithelial layer, especially the light cells, and of 'chemical signal' as an initiating modulating factor in the disturbance of Ca2+ homeostasis was suggested. It is pointed out that melanin is capable of binding calcium and may act as a buffering system. Finally, the possible malfunction of the Ca-overloaded melanocytes on the inner ear function is discussed.