Prolonged maternal exposure to glucocorticoids alters selenoprotein expression in the developing brain

Area of Science:

• Neuroscience
• Developmental Biology
• Nutritional Biochemistry

Background:

• Early life stress impacts neurodevelopment via the hypothalamic-pituitary-adrenal axis and glucocorticoid release.
• The brain's susceptibility to oxidative stress is exacerbated by elevated glucocorticoids.
• Selenium, an essential trace element, supports antioxidant defenses through selenoproteins and may mitigate oxidative damage.

Purpose of the Study:

• To investigate the hypothesis that high glucocorticoid exposure disrupts selenoprotein expression in the developing brain.
• To examine the effects of maternal corticosterone administration and varying selenium diets on offspring brain selenoprotein levels.

Main Methods:

• C57 wild-type dams were fed moderate or high selenium diets and given corticosterone in drinking water during early postnatal development (days 1-15).
• Offspring brains were analyzed using western blot to quantify levels of specific selenoproteins and the glucocorticoid receptor.

Main Results:

• Maternal corticosterone exposure increased glutathione peroxidase 1 and 4 levels in the prefrontal cortex, hippocampus, and hypothalamus.
• Corticosterone decreased glucocorticoid receptor levels in the hippocampus and increased selenoprotein W in the hypothalamus.
• High selenium diet independently reduced glucocorticoid receptor levels in offspring hippocampus and female prefrontal cortex.

Conclusions:

• Early life exposure to excess glucocorticoids alters selenoprotein expression in the developing brain.
• Dietary selenium intake influences glucocorticoid receptor levels, suggesting a modulatory role in stress response pathways.