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The maternal administration of LiCl induced follicular dilatation and degeneration, hyperplasia, lumen obliteration and colloid vacuolation in the maternal and neonatal thyroid gland at postnatal days (PNDs) 14, 21 and 28. Neuronal degeneration (spongiform), gliosis, nuclear pyknosis, perivascular oedema, and meningeal hyperaemia were observed in the neonatal cerebral cortex of the maternal LiCl\u2010treated group at examined PNDs. This disturbance appears to depend on intensification in the neonatal cerebral malondialdehyde (MDA), nitric oxide (NO), and hydrogen peroxide (H<jats:sub>2<\/jats:sub>O<jats:sub>2<\/jats:sub>) levels, and attenuation in the glutathione (GSH), total thiol (t\u2010SH), catalase (CAT), and superoxide dismutase (SOD) levels. In the neonatal cerebrum, the fold change in the relative mRNA expression of deiodinases (DII and DIII) increased significantly at PNDs 21 and 14, respectively, in the maternal LiCl\u2010treated group. These data suggest that maternal LiCl may perturb the thyroid\u2013cerebrum axis generating neonatal neurodevelopmental disorder.<\/jats:p>","DOI":"10.1002\/jdn.10151","type":"journal-article","created":{"date-parts":[[2021,9,16]],"date-time":"2021-09-16T11:04:37Z","timestamp":1631790277000},"page":"741-758","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Maternal LiCl exposure disrupts thyroid\u2013cerebral axis in neonatal albino rats"],"prefix":"10.1002","volume":"81","author":[{"given":"Dena A. 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