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Congenital Ataxia and Otolith Defects Due to Manganese Deficiency in Mice¹

Department of Nutrition, University of California, Davis, California 95616, and Department of Biological Sciences, University of Cincinnati, Cincinnati, Ohio 45221

Manganese deficiency in mice caused congenital ataxia in some progeny. The most diagnostic means of detecting the ataxia was to place all mice in a tank of water and observe their ability to maintain a normal, upright position. The incidence of ataxia increased approximately in proportion to the duration and severity of the manganese-deficient state of the mother. Cleared otic capsules revealed that otoliths were reduced in size, or were absent, in many of the manganese-deficient progeny. Supplementation of the manganese-deficient females after day 14 of gestation was ineffective in reducing the incidence of the otolithic effect. Supplementation between days 12 and 14 was only partially effective, whereas supplementation starting on day 11 was sufficient for completely normal development of otoliths. The absence of otolithic crystals is attributed to a defect in the synthesis of the organic matrix which appears to be composed of acid mucopolysaccharides. The absence of otoliths was also found in manganese-deficient chicks and presumably explains the long-standing reports of ataxia due to manganese deficiency in poultry and other domestic animals.

² Portions of this research were completed in partial fulfillment of the requirements for the Ph.D. degree in genetics, University of California, Davis, California.

³ Current address: Department of Biological Sciences, University of Cincinnati, Cincinnati, Ohio 45221.

Manuscript received 1 December 1969.

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