ArticleMolecular neurobiology2014
Developmental hypothyroxinemia and hypothyroidism reduce proliferation of cerebellar granule neuron precursors in rat offspring by downregulation of the sonic hedgehog signaling pathway.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 28 citations in OpenAlex.
- Establishment and investigation of a surgical model of hypothyroidism in Wistar rats.PloS one · 2026Article
- Emerging research themes in maternal hypothyroidism: a bibliometric exploration.Frontiers in immunology · 2024Review
- Multisensory Stimulation Improves Cognition and Behavior in Adult Male Rats Born to LT4-treated Thyroidectomized Dams.Endocrinology · 2022Article
- Sonic Hedgehog and Triiodothyronine Pathway Interact in Mouse Embryonic Neural Stem Cells.International journal of molecular sciences · 2020Article
- Clinical and subclinical maternal hypothyroidism and their effects on neurodevelopment, behavior and cognition.Archives of endocrinology and metabolism · 2020Review
- The Role of Astrocytes in the Development of the Cerebellum.Cerebellum (London, England) · 2019Review
- Transport, Metabolism, and Function of Thyroid Hormones in the Developing Mammalian Brain.Frontiers in endocrinology · 2019Review
- Iodine as Essential Nutrient during the First 1000 Days of Life.Nutrients · 2018Review
- Influence of maternal thyroid hormones during gestation on fetal brain development.Neuroscience · 2017Review
- Maternal Different Degrees of Iodine Deficiency during Pregnant and Lactation Impair the Development of Cerebellar Pinceau in Offspring.Frontiers in neuroscience · 2017Article
- Marginal Iodine Deficiency Affects Dendritic Spine Development by Disturbing the Function of Rac1 Signaling Pathway on Cytoskeleton.Molecular neurobiology · 2017Article
- Neonatal thyroid-stimulating hormone concentration and psychomotor development at preschool age.Archives of disease in childhood · 2016Article
- Gestational Hypothyroxinemia Affects Glutamatergic Synaptic Protein Distribution and Neuronal Plasticity Through Neuron-Astrocyte Interplay.Molecular neurobiology · 2016Article
- Different Degrees of Iodine Deficiency Inhibit Differentiation of Cerebellar Granular Cells in Rat Offspring, via BMP-Smad1/5/8 Signaling.Molecular neurobiology · 2016Article
- Maternal Hypothyroxinemia-Induced Neurodevelopmental Impairments in the Progeny.Molecular neurobiology · 2016Review
- Gestational and early postnatal hypothyroidism alters VGluT1 and VGAT bouton distribution in the neocortex and hippocampus, and behavior in rats.Frontiers in neuroanatomy · 2015Article
- An evo-devo approach to thyroid hormones in cerebral and cerebellar cortical development: etiological implications for autism.Frontiers in endocrinology · 2014Review
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Iodine deficiency (ID)-induced hypothyroxinemia and hypothyroidism during development result in dysfunction of the central nervous system, affecting psychomotor and motor function, although the underlying mechanisms causing these alterations are still unclear. Therefore, our aim is to study the effects of developmental hypothyroxinemia, caused by mild ID, and developmental hypothyroidism, caused by severe ID or methimazole (MMZ), on the proliferation of cerebellar granule neuron precursors (CGNPs), an excellent experimental model of cerebellar development and function. The sonic hedgehog (Shh) signaling pathway is essential for CGNP proliferation, and as such, its activation is also investigated here. A maternal hypothyroxinemia model was established in Wistar rats by administrating a mild ID diet, and two maternal hypothyroidism models were developed either by administrating a severe ID diet or MMZ water. Our results showed that hypothyroxinemia and hypothyroidism reduced proliferation of CGNPs on postnatal day (PN) 7, PN14, and PN21. Accordingly, the mean intensity of proliferating cell nuclear antigen and Ki67 nuclear antigen immunofluorescence was reduced in the mild ID, severe ID, and MMZ groups. Moreover, maternal hypothyroxinemia and hypothyroidism reduced expression of the Shh signaling pathway on PN7, PN14, and PN21. Our study supports the hypothesis that developmental hypothyroxinemia induced by mild ID, and hypothyroidism induced by severe ID or MMZ, reduce the proliferation of CGNPs, which may be ascribed to the downregulation of the Shh signaling pathway.
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