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Role of late maternal thyroid hormones in cerebral cortex development: an experimental model for human prematurity

P Berbel1, D Navarro, E Ausó

  • 1Instituto de Neurociencias, Universidad Miguel Hernández and Consejo Superior de Investigaciones Científicas, Sant Joan d'Alacant, Alicante, Spain. pere.berbel@umh.es

Cerebral Cortex (New York, N.Y. : 1991)
|October 9, 2009
PubMed

Insights

Maternal thyroid hormones (THs) are crucial for fetal brain development, even late in gestation. Treating premature neonates with thyroxine may prevent neurodevelopmental issues caused by low TH levels.

Area of Science:

  • Neuroendocrinology
  • Developmental Neuroscience
  • Perinatal Medicine

Background:

  • Hypothyroxinemia affects a significant portion of premature neonates, increasing risks of neurodevelopmental alterations.
  • Maternal thyroid hormones (THs) play a critical role in fetal brain maturation, particularly late in gestation.

Purpose of the Study:

  • To investigate the impact of late maternal hypothyroidism on offspring's cerebral maturation using an established animal model.
  • To determine if thyroxine treatment can ameliorate neurodevelopmental deficits caused by maternal hypothyroidism.

Main Methods:

  • Developed a rat model of late maternal hypothyroidism (LMH) by thyroidectomy and hormone infusion.
  • Administered thyroxine to LMH dams from embryonic day 17 to postnatal day 0.
  • Assessed offspring neurodevelopment through histological analysis (cortical lamination, neuronal migration, hippocampal organization) and behavioral testing (learning).
  • Quantified hippocampal expression of key proteins: phosphorylated cAMP response element-binding protein (pCREB) and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2).

Main Results:

  • LMH pups exhibited abnormal cortical lamination and misplaced neurons in the subcortical white matter and hippocampus.
  • Significant reduction in Zn-positive area and altered mossy fiber organization in the hippocampal CA3 region of LMH pups.
  • LMH pups demonstrated delayed learning, correlating with decreased hippocampal pCREB and pERK1/2 expression.
  • Thyroxine treatment of LMH dams successfully reversed these neurodevelopmental and molecular abnormalities.

Conclusions:

  • Maternal THs remain essential for normal offspring neurodevelopment, extending beyond the onset of fetal thyroid function.
  • The study supports the potential therapeutic benefit of thyroxine supplementation in premature neonates to counteract maternal TH deficiency.
  • This research highlights the critical window of maternal TH influence on fetal brain development and suggests a viable treatment strategy.

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