Abstract

The relationship of manganese to some aspects of brain function was studied in rats. Electroshock convulsions were produced in the following groups: 1) normal controls, 2) manganese-deficient, not ataxic, 3) manganese-deficient, congenitally ataxic, 4) not manganese-deficient, congenitally ataxic. The threshold for minimal seizures was significantly lower than normal in the two manganese-deficient groups. All manganese-deficient rats also showed alterations in the pattern of a maximal seizure. These data are interpreted to mean that brain excitability or convulsability was increased in manganese-deficient rats regardless of the presence or absence of ataxia, thus suggesting that congenital ataxia and increased convulsability are independent expressions of manganese deficiency. The convulsions and death induced by l-hydrazinophthalazine (hydralazine) in normal rats could be prevented by the prior administration of manganese salts. Cortical electroencephalographic (EEG) recordings indicated that ataxic manganese-deficient animals have a higher average EEG frequency under anesthesia than do controls. These studies suggest that the level of manganese in the body is important in determining the susceptibility of an animal to convulsive states.

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