Treadmill exercise improves neuronal survival by inhibiting apoptosis in the prefrontal cortex of congenital hypothyroid rats

Abstract

Introduction: Thyroid hormone deficiency during development can have detrimental effects on the structure and function of the nervous system. This study aimed to examine the effects of developmental thyroid hormone deficiency on neuronal survival and gene expression of pro-apoptotic Bax and anti-apoptotic Bcl-2 in the prefrontal cortex of congenital hypothyroid rats. The possible protective role of treadmill exercise was also investigated. Materials and Methods: A congenital hypothyroid model was made by treatment of pregnant Wistar rats with propylthiouracil (PTU) in drinking water from the sixth day of gestation until the end of the lactation period. Control mothers received water during this period. The male offspring were then divided into two groups with/without four weeks of treadmill exercise. Next, the animals were sacrificed and prefrontal cortices were isolated to examine neuronal survival and expression of apoptosis-related genes (Bax and Bcl-2) using cresyl violet staining and real-time polymerase chain reaction, respectively. Results: Our results demonstrated that decreased neuronal survival was associated with a significant increase in Bax and a significant decrease in Bcl-2 gene expression in congenital hypothyroid rats. Treadmill exercise was able to increase the number of surviving neurons by decreasing Bax and increasing Bcl-2 levels; however, significant differences still remained compared to the control group. Conclusion: Developmental thyroid hormone deficiency leads to neuronal damage by activating the apoptosis mechanism. Exercise can improve neuronal survival by inhibiting apoptosis in the prefrontal cortex of congenital hypothyroid rats.