Department of Integrative Physiology, Gunma University Graduate School of Medicine, 3-39-22 Showa-machi, Maebashi, Gunma, Japan.
Cerebellum. 2013 Jun;12(3):304-6. doi: 10.1007/s12311-012-0437-8.
The thyroid hormone (L-triiodothyronine (T3), thyroxine (T4)) plays a critical role in cerebellar development. Circulating T4 preferentially crosses the blood-brain barrier through several amino acid transporters. Then, it is taken up by astrocyte to convert into T3, which is a bioactive ligand for nuclear thyroid hormone receptor (TR). Liganded TR regulates the expression of target genes that may play an important role in cerebellar development and function. Thus, thyroid hormone deficiency results in the change in neuronal excitability and aberrant neurotransmitter transport, which induces abnormal motor coordination, decreased locomotor activity, and increased anxiety. In addition to genomic action of the thyroid hormone, T4 alters actin polymerization and iodothyronine deiodinase activity in astrocyte through non-genomic pathway, which may also contribute to the normal brain development. Taken together, thyroid hormone regulates cerebellar development and plasticity through multiple signal transduction pathways.
甲状腺激素（L-三碘甲状腺原氨酸（T3）、甲状腺素（T4））在小脑发育中起着关键作用。循环中的 T4 通过几种氨基酸转运体优先穿过血脑屏障。然后，它被星形胶质细胞摄取并转化为 T3，T3 是核甲状腺激素受体（TR）的生物活性配体。配体结合的 TR 调节靶基因的表达，这些靶基因可能在小脑发育和功能中发挥重要作用。因此，甲状腺激素缺乏会导致神经元兴奋性改变和神经递质转运异常，从而引起运动协调异常、运动活性降低和焦虑增加。除了甲状腺激素的基因组作用外，T4 通过非基因组途径改变星形胶质细胞中的肌动蛋白聚合和碘甲状腺原氨酸脱碘酶活性，这也可能有助于正常的大脑发育。综上所述，甲状腺激素通过多种信号转导途径调节小脑发育和可塑性。
