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Rapid Golgi Stain for Dendritic Spine Visualization in Hippocampus and Prefrontal Cortex
Published on: December 3, 2021
Marginal Iodine Deficiency Affects Dendritic Spine Development by Disturbing the Function of Rac1 Signaling Pathway
Hui Min1, Jing Dong1, Yi Wang1
1Department of Occupational and Environmental Health, School of Public Health, China Medical University, No. 77 Puhe Road, Shenyang North New Area, Shenyang, 110122, People's Republic of China.
Insights
Marginal iodine deficiency during development mildly impairs hippocampus function by affecting thyroid hormone levels. This impacts learning and memory through reduced synaptic plasticity and dendritic spine development, linked to the Rac1 pathway.
Area of Science:
- Neuroscience
- Developmental Biology
- Endocrinology
Background:
- Iodine deficiency (ID) during development impairs brain function.
- Marginal ID, characterized by low thyroxine (T4) levels, may adversely affect hippocampus development, but mechanisms are unclear.
Purpose of the Study:
- To investigate the effects of marginal ID on hippocampus development and function in Wistar rats.
- To explore the underlying mechanisms involving the Rac1 signaling pathway.
Main Methods:
- Established Wistar rat models with an ID diet during pregnancy and lactation.
- Assessed long-term potentiation (LTP) in the hippocampal CA1 region.
- Utilized Golgi-Cox staining to analyze dendritic spine development and investigated Rac1 pathway activation.
Main Results:
- Marginal ID slightly reduced LTP (f-EPSP slope and PS amplitude).
- A mild decrease in dendritic spine density was observed during critical developmental periods.
- Decreased activation of the Rac1 signaling pathway was noted in pups exposed to maternal marginal ID.
Conclusions:
- Marginal ID can lead to slight impairments in hippocampal LTP and dendritic spine development.
- These effects may be mediated by the abnormal regulation of the Rac1 signaling pathway on the actin cytoskeleton.
Abstract:
Iodine deficiency (ID)-induced thyroid hormone (TH) insufficient during development leads to impairments of brain function, such as learning and memory. Marginal ID has been defined as subtle insufficiency of TH, characterized as low thyroxine (T4) levels, whether marginal ID potentially had adverse effects on the development of hippocampus and the underlying mechanisms remain unclear. Thus, in the present study, we established Wistar rat models with ID diet during pregnancy and lactation. The effects of marginal ID on long-term potentiation (LTP) were investigated in the hippocampal CA1 region. To study the development of dendritic spines in pyramidal cells, Golgi-Cox staining was conducted on postnatal day (PN) 7, PN14, PN21, and PN28. The activation of Rac1 signaling pathway, which is essential for dendritic spine development by regulating actin cytoskeleton, was also investigated. Our results showed that marginal ID slightly reduced the field-excitatory postsynaptic potential (f-EPSP) slope and the population spike (PS) amplitude. Besides, the density of dendritic spines during the critical period of rat postnatal development was mildly decreased, and we found no significant change of spine morphology in marginal ID group. We also observed decreased activation of the Rac1 signaling pathway in pups subjected to maternal marginal ID. Our study may support the hypothesis that decreased T4 induced by marginal ID results in slight impairments of LTP and leads to mild damage of dendritic spine development, which may be due to abnormal regulation of Rac1 signaling pathway on cytoskeleton.
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