Iodine deficiency increases apoptosis and decreases synaptotagmin-1 and PSD-95 in rat hippocampus

ISSN： 1476-8305

Source： Nutritional Neuroscience, Vol.16, Iss.3, 2013-05, pp. : 135-141

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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.