Navarro D, Alvarado M, Morte B, Berbel D, Sesma J, Pacheco P, Morreale de Escobar G, Bernal J, Berbel P
Department Histology and Anatomy, Universidad Miguel Hernández, Sant Joan d'Alacant, Alicante, Spain.
Department Histology and Anatomy, Universidad Miguel Hernández, Sant Joan d'Alacant, Alicante, Spain Instituto de Neuroetología, Universidad Veracruzana, Xalapa, Veracruz 91100, México.
Cereb Cortex. 2014 Oct;24(10):2694-706. doi: 10.1093/cercor/bht129. Epub 2013 May 16.
Maternal thyroid hormones (THs) are essential for normal offspring's neurodevelopment even after onset of fetal thyroid function. This is particularly relevant for preterm children who are deprived of maternal THs following birth, are at risk of suffering hypothyroxinemia, and develop attention-deficit/hyperactivity disorder. Expression of neocortical Ca(2+)/calmodulin kinase IV (Camk4), a genomic target of thyroid hormone, and nuclear receptor-related 1 protein (Nurr1), a postnatal marker of cortical subplate (SP) cells, was studied in euthyroid fetuses and in pups born to dams thyroidectomized in late gestation (LMH group, a model of prematurity), and compared with control and developmentally hypothyroid pups (C and MMI groups, respectively). In LMH pups, the extinction of heavy Camk4 expression in an SP was 1-2 days delayed postnatally compared with C pups. The heavy Camk4 and Nurr1 expression in the SP was prolonged in MMI pups, whereas heavy Camk4 and Nurr1 expression in layer VIb remains at P60. The abnormal expression of Camk4 in the cortical SP and in layer VIb might cause altered cortical connectivity affecting neocortical function.
母体甲状腺激素（THs）对正常后代的神经发育至关重要，即使在胎儿甲状腺功能开始之后也是如此。这对于早产儿童尤为重要，他们出生后会缺乏母体THs，有患低甲状腺素血症的风险，并会发展为注意力缺陷多动障碍。在甲状腺功能正常的胎儿以及妊娠晚期接受甲状腺切除的母鼠所生的幼崽（LMH组，早产模型）中，研究了甲状腺激素的基因组靶点新皮质钙/钙调蛋白激酶IV（Camk4）和皮质下板（SP）细胞的出生后标志物核受体相关蛋白1（Nurr1）的表达，并与对照组和发育性甲状腺功能减退的幼崽（分别为C组和MMI组）进行比较。与C组幼崽相比，LMH组幼崽出生后SP中Camk4重表达的消失延迟了1 - 2天。MMI组幼崽中SP内Camk4和Nurr1的重表达延长，而VIb层中Camk4和Nurr1的重表达在P60时仍存在。皮质SP和VIb层中Camk4的异常表达可能会导致皮质连接改变，影响新皮质功能。
