Late Maternal Hypothyroidism Alters the Expression of Camk4 in Neocortical Subplate Neurons: A Comparison with Nurr1 Labeling. (16th May 2013)

• Record Type: Journal Article
• Authors: Navarro, D.; Alvarado, M.; Morte, B.; Berbel, D.; Sesma, J.; Pacheco, P.; Morreale de Escobar, G.; Bernal, J.; Berbel, P.
• Is Part Of: Cerebral cortex. Volume 24:Number 10(2014:Oct.)
• Page Start: 2694
• Page End: 2706
• Publication Date: 2013-05-16
• Subjects: attention-deficit/hyperactivity disorder -- developmental neurological diseases -- hypothyroxinemia -- preterm encephalopathy -- schizophrenia; Cerebral cortex -- Periodicals; Brain -- Periodicals; 612.825
• DOI: 10.1093/cercor/bht129
• Languages: English
• ISSNs: 1047-3211

Abstract

Abstract : 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.