Changes in MAP-2 and GFAP immunoreactivity in pup hippocampus during prepubertal and pubertal periods caused by maternal subclinical hypothyroidism

ABSTRACT

An absence of the thyroid hormone during the critical period of brain development causes delayed maturation of glial cells and neurons and decreases the number of hippocampal cells. This study aims to examine the impact of maternal subclinical hypothyroidism (SCH) on pup hippocampus during the prepubertal and pubertal periods by means of assessing the histopathological changes in astrocytes and neurons.Twelve Wistar albino pregnant rats were divided into two groups, Group H and Group C. Group C was designated as the control group and nothing was added to their drinking water. SCH was induced in Group H by administering 6-propyl-2-thiouracil (PTU) at a final concentration of 0.01% in the drinking water of pregnant rats for 21 days. Male pups for each group were divided evenly and evaluated on either day 15 (prepubertal) or 60 (pubertal) (7 pups in each group). At the end of the experimental period, the rats were sacrificed for analysis of brain tissue. Immunoreactivity intensities of MAP-2 and GFAP were evaluated in hippocampus tissue. Thyroid function was determined using ELISA. The structure of hippocampus was evaluated by hematoxylin-eosin staining. Finally, the TUNEL method was utilized to show apoptosis of hippocampus tissue. The results were analyzed statistically.The findings show that maternal SCH causes disruption in hippocampal cytoskeleton and dendritic organization, especially during the pubertal period, as well as a decrease in MAP-2 expression. We observed structural deformation in astrocytes, reduced astrocyte survival and GFAP expression. Finally, we found that the number of neuronal apoptotic cells tended to increase in the pubertal period

RESUMEN

No disponible