目的观察碘缺乏及甲状腺功能减退大鼠仔鼠小脑发育的影响,以及对CaMKⅡ表达的影响。方法雌性Wistar大鼠,交配妊娠后,取孕鼠28只按体重随机分成对照组、甲状腺功能减退-1组、甲状腺功能减退-2组和碘缺乏组。自妊娠第6日起,对照组继续饲以普通饲料;甲减-1组、甲减-2组分别给予5ppm、15ppm丙基硫尿嘧啶饮水,饲以普通饲料;碘缺乏组饲以缺碘地区粮食配制的饲料,至仔鼠生后第28天(PN28)。PN7、PN14、PN21、PN28、PN42取仔鼠小脑皮质进行尼氏染色及CaMKⅡ蛋白免疫组化染色。结果 PN14、PN21、PN28及PN42各组大鼠仔鼠小脑神经元的尼氏小体的平均积分光密度值显著低于对照组,具有统计学意义(P〈0.05);仔鼠小脑皮质CaMKⅡ表达均显著低于对照组,具有统计学意义(P〈0.05)。结论碘缺乏和甲状腺功能减退可影响大鼠仔鼠小脑CaMKⅡ蛋白的表达,从而损害仔鼠小脑,导致脑神经发育障碍。
Objective We have tested whether congenital iodine deficiency and hypothyroidism could regulate expression of CaMKⅡin pup cerebellum cortex,and impair functional lesion in pup cerebellum.Methods Female Wistar rats(n=28) after pregnancy were randomly divided into four groups: control group,iodine deficient group,hypothyroid-1 group(5 ppm) and hypothyroid-2 group(15 ppm).The control group was fed a normal diet during the experiment.The iodine deficient group was fed an iodine-deficient diet.The hypothyroid-1 group was fed a normal diet and had 5 ppm PTU-added water and the hypothyroid-2 group had 15 ppm PTU-added water.All the groups were from GD6 through to postnatal day(PN) 28.On PN7,PN14,PN21,PN28,pups in each group the part of the cerebellum were separated from the brain for protein detection by Nissl's staining and CaMKⅡimmunohistochemistry.Results On PN14,PN21,PN28 and PN42,Nissl's body expression in 5 ppm,15 ppm and iodine-deficient groups were significantly lower than those of controls(P〈0.05);CaMKⅡexpression in 15 ppm and iodine-deficient groups were significantly lower than those of controls(P〈0.05).Conclusion Iodine deficiency and hypothyroidism during a period of brain development changed cerebellar morphology and affected the expression of CaMKⅡ.The changes could impair synaptic plasticity,affect the formation of normal neural circuit,and resulted in cerebellar development disturbance.