ArticleScientific reports2021
Thyroid hormone insufficiency alters the expression of psychiatric disorder-related molecules in the hypothyroid mouse brain during the early postnatal period.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- An ASXL3-thyroid hormone axis in parvalbumin interneurons controls autism-like behaviors.Science advances · 2026Article
- Increased Absorption of Thyroxine in a Murine Model of Hypothyroidism Using Water/COInternational journal of molecular sciences · 2024Article
- Thyroid hormone as a temporal switch in mouse development.European thyroid journal · 2023Review
- Mating experiences with the same partner enhanced mating activities of naïve male medaka fish.Scientific reports · 2022Article
- Histological, functional and transcriptomic alterations in the juvenile hippocampus in a mouse model of thyroid hormone resistance.European thyroid journal · 2022Article
- Non-Cell-Autonomous Factors Implicated in Parvalbumin Interneuron Maturation and Critical Periods.Frontiers in neural circuits · 2022Review
- The Vulnerability of the Developing Brain: Analysis of Highly Expressed Genes in Infant C57BL/6 Mouse Hippocampus in Relation to Phenotypic Annotation Derived From Mutational Studies.Bioinformatics and biology insights · 2022Article
- Review
- Congenital Hypothyroidism and Brain Development: Association With Other Psychiatric Disorders.Frontiers in neuroscience · 2021Review
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The functional role of thyroid hormone (TH) in the cortex and hippocampus of mouse during neuronal development was investigated in this study. TH insufficiency showed a decrease in the expression of parvalbumin (PV) in the cortex and hippocampus of pups at postnatal day (PD) 14, while treatment with thyroxine from PD 0 to PD 14 ameliorated the PV loss. On the other hand, treatment with antithyroid agents in adulthood did not result in a decrease in the expression of PV in these areas. These results indicate the existence of a critical period of TH action during the early postnatal period. A decrease in MeCP2-positive neuronal nuclei was also observed in the cortical layers II-IV of the cerebral cortex. The brains were then stained with CUX1, a marker for cortical layers II-IV. In comparison with normal mice, CUX1 signals were decreased in the somatosensory cortex of the hypothyroid mice, and the total thickness of cortical layers II-IV of the mice was lower than that of normal mice. These results suggest that TH insufficiency during the perinatal period strongly and broadly affects neuronal development.
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