Description:
Abstract:Hypothyroidism of mild intensity was obtained with prenatal and neonatal submission of Long‐Evans rats to an iodide‐rich diet. Chronic daily administration of methimazole to iodide‐supplemented Long‐Evans pups or to iodine‐deprived Charles‐River rats through the first 29–30 days of age provoked severe hypothyroidism. Monoamine oxidase type A (MAO‐A) and not type B (MAO‐B) activity was consistently, although slightly (by approximately 20%), increased in the hypothyroid brain. Triiodothyronine (T3)‐induced hyperthyroidism did not affect MAO activity. Replacement therapy with T3 did not normalize MAO‐A activity in hypothyroidism. Methimazole displayed a competitive and reversible in vitro inhibition of MAO‐A but not MAO‐B activity. Although this effect was obtained at concentrations far higher than those estimated to reach the brain after a single injection of the goiterogen, the occurrence of accumulation processes in the metabolism‐deficient hypothyroid neonate rs cannot be excluded. Thus, MAO‐A activity might be either directly depressed during the goiterogenic treatment, or increased as the result of some kind of rebound effect after interruption of methimazole administration.