IMPACT OF PRENATAL ALCOHOL EXPOSURE AND EARLY THYROID INTERVENTION ON BRAIN DEVELOPMENT IN NEONATAL RATS: IMPLICATIONS FOR EARLY ATHLETIC TRAINING PROGRAM

Authors

  • Jin Zhaoling Department of Neonatology, Affiliated Hospital of Yanbian University, Yanji 133000, China.
  • Li Huiwen Department of Neonatology, Affiliated Hospital of Yanbian University, Yanji 133000, China.
  • Yan Min Changchun Children's Hospital, Changchun 130000, China.
  • Quan Guangxiong Changchun Children's Hospital, Changchun 130000, China.
  • Jin Fu Department of Neonatology, Affiliated Hospital of Yanbian University, Yanji 133000, China.

Keywords:

drinking alcohol during pregnancy; Newborn rats; Brain development; Exogenous thyroxine; BDNF

Abstract

Objective: This study investigates the impact of maternal alcohol consumption during pregnancy on brain development in neonatal rats, and evaluates the potential mitigating effects of early-stage exogenous thyroxine administration. Methods: Sprague-Dawley rats were assigned to three groups: a normal control group (N), an alcohol-exposed group (A), and an alcohol-exposed group treated with thyroxine (A+T). From gestation day 6, groups A and A+T received 20ml of 22% alcohol daily, while group N received a caloric equivalent in 8% sugar-containing milk powder. From days 1 to 10 post-birth, groups N and A received subcutaneous saline injections, and group A+T received 5.0 ug/kg of thyroxine daily. We monitored body weight and blood thyroxine levels at 7-, 14-, 21-, and 28-days post-birth. The morphology and distribution of BDNF-positive neurons in the cerebral cortex were assessed by immunohistochemistry, and BDNF mRNA expression levels were quantified using RT-PCR. Results: Thyroxine levels in group A were significantly lower than those in groups N and A+T at all measured time points (P<0.05). The body weight of group A rats was consistently lower than that of groups N and A+T, with no significant difference between groups A+T and N from P21 to P28. By P7, group A+T exhibited mature BDNF-positive neuronal development similar to group N, unlike group A, which showed a significant decrease in BDNF-positive neurons by P21. BDNF mRNA levels in group A+T were significantly higher than in group A from P7 onwards (P<0.05). Conclusion: Early administration of exogenous thyroxine can counteract the detrimental effects of fetal alcohol exposure by improving hypothyroxinemia and enhancing BDNF synthesis in neonatal rats. This intervention promotes normal brain development, suggesting potential applications in improving developmental outcomes in children exposed to alcohol in utero. The implications for long-term cognitive functions and physical capabilities in athletic settings warrant further exploration, highlighting the need for focused developmental strategies in sports medicine.

Published

2024-02-01