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Nutr Neurosci. 2013 May;16(3):135-41. doi: 10.1179/1476830512Y.0000000040. Epub 2012 Dec 6.

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

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Department of Occupational and Environmental Health, School of Public Health, China Medical University, Shenyang, P R China.



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.


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.


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).


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.

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