Mucopolysaccharide synthesis in the developing inner ear of manganese-deficient and pallid mutant mice.

Abstract

AbstractHistological development of otoliths was examined in the ears of fetal Mn‐deficient and pallid mutant mice and controls. As judged by 35S incorporation, sulfomucopolysaccharides of the otolithic membrane were secreted by cells in the macular epithelium of the utriculus and sacculus. Normal development of otoliths occurred between days 15 and 16 of gestation and was indicated by the appearance of fine granules of calcium carbonate associated with a metachromatic, PAS‐positive material which specifically incorporated 35S. Manganese deficiency or the pallid gene caused reduced incorporation of 35S in the macular cells, the formation of a nonmetachromatic, variably PAS‐positive matrix which did not contain 35S, and failure of otolithic calcification. Rate‐limiting effects of manganese deficiency on sulfomucopolysaccharide synthesis by periotic chondrocytes were observed, but 35S metabolism in cartilage was unaffected by the pallid gene. The possible role of manganese production of the otolithic defect is discussed.