The Effect of Experimentally Induced Maternal Hypothyroidism on GFAP and S100B Protein Expression in Fetal Brain Tissue at 10, 15th Gestational Days and Newborn Period

Thyroid hormone is very important in central nervous system development. Thyroidhormone deficiency in critical periods of central nervous system causes glial cells and neuronsmaturation delays. It is well known that maternal hypothyroidism causes psychomotor andmental retardation in offsprings. Thyroid hormones have important functions in survival,division and differentiation of both neuronal and glial precursor cells. It was reported thatS100B and Glial Fibrillar Acidic Protein (GFAP) were good markers showing astrocytematuration. S100B and GFAP levels were found to be lower in astrocyte maturation defects.There are so many trials related to the effect of maternal hypothyroidism on central nervoussystem development, but there are few that related to the effect of maternal hypothyroidismon glial proteins. The effect of maternal thyroid hormones on glial proteins is not knownduring pregnancy. We aimed to evaluate the effect of maternal hypothyroidism on GFAP andS100B proteins expression by the way astrocyte maturation on fetal brain at 10, 15th days andnewborn period.Fifteen experimentally hypothyroid rats and 15 normal rats (control group) wereincluded to experimental study. Both groups were divided into 3 subgroups as 10, 15thgestational days and newborn. S100B and GFAP levels were studied in brain of fetus at 10,15 gestational days and newborns by Western Blot method. S100B protein and GFAP levelswere found significantly lower in brain tissues of hypothyroid mother offsprings with respectto control group.Our study showed that maternal hypothyroidism might cause changes in GFAP andS100B protein expression in central nervous system. These changes may have a role inastrocyte maturation retardation. It was observed that there are neuronal and glial changes andsevere astrocyte maturation retardations in the fetal brain development of hypothyroidmother?s offsprings.