THYROID EFFECTS ON DEVELOPING SYMPATHETIC NERVOUS SYSTEM

在实验动物中，无论是剥夺甲状腺激素还是产前 据报道，甲状腺功能减退症对生化和 交感神经系统(SNS)的形态发育。至 到目前为止，在细胞和分子水平上还没有关于 甲状腺激素发挥这些作用的机制(S)。该计划的目标是 目前的建议是确定行动的关键时间段 甲状腺激素在SNS发生发展中的作用 甲状腺激素的作用是导致这种发育的原因。最后， 甲状腺激素与神经生长的独立或整合机制(S) 将在SNS的个体发育过程中研究因子的作用。 众所周知，神经生长因子是生长和成熟所不可缺少的。 自主神经系统交感去甲肾上腺素能神经元 用于开发的早期阶段和维护 这些自主神经细胞一生中的分化状态 跨度。我们的方法将包括在小鼠身上进行实验研究 诱导性甲状腺功能减退以及遗传性甲状腺功能减退的突变小鼠。 以小鼠颈上神经节(SCG)为模型。 这些关于SNS发展的研究。

In experimental animals, both thyroid hormone deprivation and prenatal hypothyroidism are reported to influence importantly the biochemical and morphological development of the sympathetic nervous system (SNS). To date, nothing is known at the cellular and molecular levels about the mechanism(s) by which thyroid hormones exert these effects. The aims of the present proposal are to determine the critical time period for the action of thyroid hormones on SNS development and to identify the loci of the thyroid hormone actions responsible for this development. Finally, the independent or integrated mechanism(s) of thyroid hormone and nerve growth factor action will be studied during ontogenetic development of the SNS. Nerve growth factor is known to be indispensible for growth and maturation of sympathetic noradrenergic neurons of the autonomic nervous system during early stages of their development and for the maintenance of the differentiated state of these autonomic neurons throughout their life span. Our approach will include studies in mice with experimentally induced hypothyroidism as well as mutant mice with genetic hypothyroidism. The mouse superior cervical ganglion (SCG) will be used as the model for these studies of SNS development.