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Abstract
Objective
Developmental iodine deficiency (ID) leads to inadequate thyroid hormone that impairs the development of the central nervous system with an unclear mechanism. Here, we show that hippocampal apoptosis, synaptotagmin-1, and PSD-95 are involved in the synaptic impairment following developmental ID.
Methods
Two developmental rat models were created by administrating dam rats with either iodine-deficient diet or propylthiouracil (PTU, 15 ppm)-added drinking water from gestational day 6 till postnatal day (PND) 28. Then, the apoptosis in the hippocampus was determined by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, and the levels of synaptotagmin-1 and PSD-95 were detected with western blot on PND14, PND21, and PND28.
Results
The results showed that apoptosis cells and activity of caspase3 were increased in the iodine-deficient and PTU-treatment rats (P < 0.05, respectively). The iodine-deficient and PTU-treatment pups showed significantly lower level of synaptotagmin-1 and PSD-95 in hippocampus than that of controls (P < 0.05, respectively).
Conclusion
Developmental ID resulted in the increase and delay of cell apoptosis and the decrease of synaptotagmin-1 and PSD-95 in the hippocampus, which were implicated in the impairment of brain development.
Acknowledgements
This work was supported by the National Natural Science Foundation of China (grant number 81102126) and the Specialized Research Fund for the Doctoral Program of Higher Education of China (grant number20092104120025).