母体正常甲状腺素(TH)水平对胎儿神经发育至关重要。文献报道孕期临床甲状腺功能减退(CH)可干扰胚胎神经干细胞(NSCs)的分化与迁移而影响神经发育。亚临床甲状腺功能减退(SCH)，作为CH的前期阶段，其在我国妊娠妇女中的发病率为4%；但是妊娠期SCH对子代神经发育的影响目前尚不明确，且无关于妊娠期SCH影响子代NSCs增殖、分化、迁移和凋亡并引起子代神经行为和学习记忆能力受损的系列研究。本研究拟利用大鼠妊娠期SCH模型，从整体水平的一般生理发育指标观察、神经行为和学习记忆能力测试，到组织、细胞水平的NSCs增殖、分化、迁移和凋亡的分析以及调控上述过程的分子机制研究等，多个方面阐释妊娠期SCH对子代神经发育的影响及相关机制。本研究的完成将有助于深入认识妊娠期SCH及其可能存在的对子代神经发育的危害性，为临床上制定该病的筛查及诊疗方案提供科学依据，从而提高出生人口质量。

Maintenance of normal maternal thyroid function is vital for the development of fetal nervous system. Studies showed clinical hypothyroidism (CH) during pregnancy affected neurodevelopment of offspring by interfering the development of embryonic neural stem cells (NSCs). Subclinical hypothyroidism (SCH), as the early presentation of CH, accounts for 4% of pregnant women in China. It is unclear whether gestational SCH damages neurobehavioral, learning and memory abilities in offspring by affecting proliferation, apoptosis, differentiation and migration of NSCs. This study intends to use the rat gestational SCH model. First, observe the general physiological index, neural behavior and the ability of learning and memory from the overall level; second, study the proliferation, differentiation, migration and apoptosis of NSCs in tissue and cell level; third, study on the mechanism of controlling the above process from molecular level. Through these multi-perspective methods, it will explain the pregnancy effect of SCH neurobehavioral development of the offspring and the related mechanisms. Our results will help better understanding gestational SCH, as well as its potential harm on fetal nervous development and may provide new scientific basis for screen and treatment of the disease，and to improve the quality of newborns.