Elevated levels of glucocorticoids in the perinatal period of ontogeny may provoke further development of neuropathology, whose mechanisms can involve apoptosis of brain cells caused by impaired expression of neurotrophins, including the practically unstudied neurotrophic factor 3 (NT3). In order to clarify this issue, we explored the effect of glucocorticoid dexamethasone (DEX) on the NT3 and the key apoptotic protease caspase-3, mRNA levels as well as immature (proNT3) and mature (matNT3) forms of the investigated neurotrophin in the hippocampus of 3-4-day-old rats 6 or 24 hours after DEX administration. In 6 hours but not in 24 hours DEX increased the NT3 mRNA levels in the whole hippocampus, as well as the proNT3 and matNT3 proteins contents the CA1-3 fields and the dentate gyrus of the structure. In this case, the expression of apoptogenic proNT3 temporarily predominated over matNT3; however, this was not accompanied by an increase in the caspase-3 mRNA level.
- MESSENGER-RNA EXPRESSION
- ANTENATAL CORTICOSTEROIDS