Manganese Deficiency in Rats: Congenital Nature of Ataxia

Abstract

Female rats maintained from weaning on a manganese-deficient fresh milk ration were able to bear young not differing greatly in number or birth weight from those produced by females receiving a similar diet containing added manganese. Survival of the young was significantly decreased by the deficiency, and most of the surviving deficient young exhibited a pronounced ataxia, with lack of equilibrium, head retraction and tremor. Analyses of brain acetylcholinesterase activity in the young from the 19th day of gestation to 28 days after birth did not reveal any effect of manganese deficiency upon this enzyme. Both normal and manganese-deficient young showed a rise in brain acetylcholinesterase activity from birth to 21 days of age. Manganese-deficient females producing defective young were supplemented with manganese at various times during a subsequent pregnancy. Manganese supplementation begun on or before the 14th day of gestation was completely effective in preventing ataxia in the young. When manganese was withheld until the 18th day of gestation (but continued thereafter) survival was low, and all of the surviving young were ataxic. Manganese supplementation begun on the 15th or 16th days of gestation resulted in the birth of young about one-half of which were mildly ataxic. These data indicate that an irreversible congenital defect resulting in ataxia occurs between the 14th and 18th days of gestation in manganese-deficient female rats.