Introduction: Nervous system growth and differentiation are intimately interrelated with the presence of thyroid hormones (THs) in early development stages. Hypothyroidism during the fetal and postnatal life results in an irreversible mental retardation syndrome. Aim of the study: Assessment of the effect of 3,5,3’-triiodo-L-thyronine (T3) on changes in the cerebral neurotransmitters level in hypothyroid rats male offspring and the possible role of Na+, K+-ATPase activity. Materials and methods: Hypothyroidism during pregnancy and lactation in one group (hypothyroid group) was induced by the antithyroid drug, methimazole (MMI) that was added to drinking water at a concentration of 0.02%. In the second group (T3-treated hypothyroid group), MMI was stopped and animal's offsprings were given T3 (20 μg/100 g body weight in 0.01 N NaOH, i.p.) for one week. The third group is the control group; neither the mother nor the offspring received any drug. The hypothyroid state in mothers during pregnancy was confirmed by measuring total thyroxine (TT4) and total triiodothyronine (TT3) at gestational day 10. At the end of experiment, the offsptings were sacrificed and free thyroxine (FT4) and free triiodothyronine (FT3) in sera and neurotransmitters (dopamine, norepinephrine and serotonin) and Na+, K+-ATPase activity were measured in the cerebral homogenate. Results: Maternal hypothyroidism induced a significant decrease in the cerebral level of dopamine, norepinephrine, serotonin and Na+, K+-ATPase activity when compared with euthyroid group. Treatment with T3 significantly increased the cerebral level of neurotransmitters and Na+, K+-ATPase activity when compared with the hypothyroid group. Conclusion: T3 supplementation during the postnatal period through its effect on the cerebral Na+, K+-ATPase effectively reversed the effect of maternal methimazole-induced hypothyroidism on the cerebral level of dopamine, norepinephrine and serotonin.
