Developmental Iodine Deficiency and Hypothyroidism Reduce Phosphorylation of Calcium/Calmodulin-Dependent Kinase II in the Rat Entorhinal Cortex |
| |
Authors: | Yi Wang Yi Hou Jing Dong Hongde Xu Jian Gong Jie Chen |
| |
Institution: | (1) Department of Occupational and Environmental Health, School of Public Health, China Medical University, 92 North 2nd Road, Shenyang, 110001, People’s Republic of China; |
| |
Abstract: | Iodine is essential for the synthesis of triiodothyronine (T3) and thyroxine (T4). Iodine deficiency leads to inadequate thyroid hormone. Hypothyroidism induced by iodine deficiency during gestation and
postnatal period leads to cognitive deficits in learning and memory. However, the mechanism underlying these deficits is unclear.
Calcium-dependent calmodulin kinase II (CaMKII) known as a potential memory molecule regulates important neuronal functions
including learning and memory. Recent studies have shown that hypothyroidism alters phosphorylation of CaMKII in hippocampus
or even in sympathetic ganglia of rats. Though the entorhinal cortex (EC) is an important functional structure within the
neuronal network responsible for learning and memory, little is known about the effect of hypothyroidism on phosphorylation
of CaMKII in the EC. Here, we report that iodine deficiency and propylthiouracil treatment through gestation and lactation
reduce phosphorylation of CaMKII in the EC of pups. The increase of calcineurin, as well as reduction of neurogranin and calmodulin,
may account for the reduced phosphorylation of CaMKII induced by developmental iodine deficiency and hypothyroidism. These
findings in the EC may contribute to understanding the mechanisms that underlie impairment of learning and memory induced
by developmental iodine deficiency and hypothyroidism. |
| |
Keywords: | |
本文献已被 SpringerLink 等数据库收录! |
|