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Effect of maternal excessive iodine intake on neurodevelopment and cognitive function in rat offspring

Le Zhang12, Weiping Teng12*, Yuhui Liu2, Jing Li12, Jinyuan Mao2, Chenling Fan2, Hong Wang2, Hongmei Zhang2 and Zhongyan Shan12*

Author Affiliations

1 Department of Endocrinology and Metabolism, First Affiliated Hospital of China Medical University, Shenyang 110001, People’s Republic of China

2 Endocrinology Institute of China Medical University, Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, People’s Republic of China

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BMC Neuroscience 2012, 13:121  doi:10.1186/1471-2202-13-121

Published: 8 October 2012



Iodine deficiency and iodine excess are both associated with adverse health consequences. Iodine deficiency during pregnancy leads to insufficient maternal thyroid hormone, subsequently causing irreversible adverse effects on the neurological and cognitive functions of the offspring. The results of our previous epidemiological study suggested that mild iodine excess might increase the prevalence of subclinical hypothyroidism. In the present study, female Wistar rats maintained on low-iodine grain were randomly assigned to three groups based on iodated water concentration: low iodine (LI, 1.2 μg/d), normal iodine (NI, 5–6 μg/d), and 3-fold high iodine (3HI, 15–16 μg/d). The present study investigated whether higher-than-normal iodine intake (3HI) by rats from before pregnancy until breastfeeding affects the postnatal (PN) neurodevelopment (PN7 and PN45) of their offspring during particularly sensitive periods in brain development.


After 12 weeks of treatment (before pregnancy), iodine concentrations in urine and thyroid tissue and circulating thyroxine of adult females correlated with iodine intake. Brain-derived neurotrophic factor (BDNF) expression in the hippocampi of pups on PN7 and PN45 was decreased in 3HI group compared to the NI controls (P < 0.05, all) On PN7 and PN45, the BDNF levels of the 3HI pups were 83.5% and 88.8%, respectively, that of the NI pups. In addition, the 3HI group had a higher neuroendocrine-specific protein A (NSP-A) level than the NI controls on PN7 (P < 0.05). NSP-A levels of the 3HI pups were 117.0% that of the NI pups. No significant difference was observed in the expressions of c-Fos or c-Jun in the hippocampal CA1 region of the 3HI group compared to the controls (P > 0.05). Results from the Morris water maze test revealed that pups of the 3HI group had mild learning and spatial memory deficits.


The neurodevelopmental and cognitive deficits of the 3HI pups were mild and temporary, likely related to the changes in hippocampal protein expressions of BDNF and NSP-A.

Iodine deficiency; Iodine excess; Thyroid hormone; Hippocampus; Neurodevelopment