AI Article Synopsis
- Certain developmental neurotoxicants can disrupt thyroid hormone levels, crucial for brain development in both humans and animals, with propylthiouracil (PTU) used to induce hypothyroidism in rats for research.
- The study focused on eight genes related to neural network formation, particularly observing changes in mRNA levels of genes like BDNF and NMDA receptors in the cerebellum of PTU-treated rats on postnatal day 22.
- Findings showed that PTU increased NR2B mRNA while decreasing NR2A and BDNF, indicating a potential delay in the normal maturation of NMDA receptor subunits during brain development.
Article Abstract
Certain kinds of developmental neurotoxicants are considered to act by affecting the levels of thyroid hormones, which are essential for the brain development of both humans and experimental animals. Hypothyroidism experimentally induced in rats with propylthiouracil (PTU) offers a useful animal model for developmental neurotoxicity. The purpose of the present study was to clarify developmental alterations in gene expression caused by PTU in this model, with the focus on eight genes implicated in neural network formation or synaptic functions, such as the brain-derived neurotrophic factor (BDNF) and NMDA receptors 2A/2B. First, we measured the developmental profile of gene expression in vehicle-dosed rat cerebellum by quantitative RT-PCR and then examined the effects of PTU on mRNA levels on postnatal day (PND) 22, when most of the cerebellar structures in mature animals are already formed. PTU induced up-regulation of NR2B mRNA and down-regulation of NR2A and BDNF mRNAs in the cerebellum on PND 22, but there were no changes in the other genes (growth associated protein-43, L1, neuronal cell adhesion molecule, synaptophysin, post synaptic density-95). Examination of the effects of PTU on maturation of NMDAR subunits (NR2A/NR2B) demonstrated changes in relative expression on PND 14, but not on PND 4, with recovery after maturation. The profile of NMDAR subunits in vehicle-dosed rats showed a shift from NR2B to NR2A during development. These results suggest PTU can delay this switching from NR2B to NR2A subunits in the maturation of NMDA receptors.
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| http://dx.doi.org/10.1016/j.neuro.2005.11.008 | DOI Listing |
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