The effects of experimental perinatal hypothyroidism and thyrotoxicosis on neural plasticity and memory

thyroid hormone has a crucial role at development of central nervous system. Atthe critical phase of brain development, absence of thyroid hormone leads to delay inmaturation of glial cells and neurons. It is well known that at the presence of maternalhypothyroidism, psychomotor improvement of children and the level of IQ stay behind.Studies pointed out that cell adhesion molecules have very important roles on growingof brain and synaptic plasticity. Neural plasticity has important roles upon function ofbrain, learning, and formation of memory. For differentiation of cortical neurons andincreasing the activities of synaptic plasticity, the powerful secretion of adhesionmolecules of nerve cells are required. It is known that absence of thyroid hormonecauses to abnormalities at synthesis and release of adhesion molecules.Investigators have been focused upon maternal hypothyroid then hyperthyroidbecause hypothyroid is more common. However, studies investigating the effect ofhypothyroidism upon neural cell adhesion molecules are scarce. At the period ofpregnancy the increment in maternal thyroid hormones increases the risk ofpreeclampsia, pre-term delivery and low birth weight. But there aren?t enoughresearches about the effect of hyperthyroidism on neural plasticity and learning.In our study we aimed to point out the effects of maternal thyroid dysfunctionsupon neural plasticity and learning of newborn animal during the whole period ofpregnancy and two weeks after the term.For experimental practising; fifteen newborn rats were taken; five mother withnormal thyroid functions, five with hypothyroidism and five with thyrotoxicosis. Forlearning test, a widely used and accepted test, the Morris Water Maze test, was used.Neural cell adhesion molecules were studied by the method of Western Blot.At the control and thyrotoxicosis group it was seen that learning increases dayby day from first day to fifth day. The control and thyrotoxicosis groups found theplatform starting from the first day. In hypothyroid group, only one animal found theplatform in first two days. In third and fourth day two animals found the platform andthe fifth day three of animal found the platform. And it was understood that sufficientlearning day by day was not realized.Relative intensity of NCAM izoforms (NCAM120, NCAM140, and NCAM180)were comparable in control and thyrotoxicosis group. The rates of NCAM120,NCAM140 determined were similar in the entire group, but NCAM180?s leveldetermined was higher in the hypothyroid group then the others.Results of our study show that the insufficiency of maternal thyroid hormoneprevents the maturation of central neural system and causes the incapacities of learningand memory. Our study points out that the expressions of NCAM izoforms changed.The brain of young rats with a hypothyroid mother was not well developed, andlearning and the enhancement of memory functions were worse then the control group.Finally it is obvious that the maternal thyroid effects the young animal?s psychomotordevelopments badly.Key words: Maternal thyroid dysfunctions, neural plasticity, NCAM andlearning.