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Thyroid Hormone Economy in the Perinatal Mouse Brain: Implications for Cerebral Cortex Development
Soledad Bárez-López1,2, Maria Jesus Obregon1, Juan Bernal1,2
1Department of Endocrine and Nervous System Pathophysiology, Instituto de Investigaciones Biomédicas Alberto Sols, Consejo Superior de Investigaciones Científicas (CSIC)-Universidad Autónoma de Madrid (UAM), E-28029 Madrid, Spain.
Cerebral Cortex (New York, N.Y. : 1991)
|April 14, 2017
Summary
Maternal thyroid hormone (T4) crosses the placenta, and fetal brain converts T4 to T3 via type-2 deiodinase (D2) at the blood-cerebrospinal fluid barrier for neurodevelopment.
Area of Science:
- Neuroscience
- Endocrinology
- Developmental Biology
Background:
- Thyroid hormones (THs) are crucial for fetal neurodevelopment.
- Mechanisms of T3 brain delivery during mouse fetal development are poorly understood.
Purpose of the Study:
- Investigate the sources of brain T3 during mouse fetal development.
- Elucidate the role of T4 to T3 conversion in the developing brain.
Main Methods:
- Biochemical analyses
- Anatomical studies
- Molecular approaches
Main Results:
- Fetal brain T4 is largely of maternal origin during late gestation.
- Type-2 deiodinase (D2) activity converts fetal T4 to T3 in the developing brain.
- D2 is essential for T3-dependent gene expression and regulating cerebral cortex TH levels.
- Dio2 expression is concentrated at the blood-cerebrospinal fluid barrier (BCSFB).
Conclusions:
- T4 conversion by D2 at the BCSFB is the primary source of brain T3 during neocortical development.
- This mechanism ensures adequate active thyroid hormone supply for fetal brain development and homeostasis.