The effects of glucocorticoids on the ratio between brain-derived neurotrophic factor and its proform in the neonatal hippocampus

Hydrocortisone, which activates both mineralo- and glucocorticoid receptors, decreased the levels of the proform of the brain-derived neurotrophic factor (proBDNF), which induces apoptosis, and mature BDNF (mBDNF), which promotes the survival of brain cells, in the hippocampus of 8-day-old rats 6 h after drug administration. A shift in the mBDNF/proBDNF ratio to the prevalence of the antiapoptotic form of neurotrophin in the hippocampus after hormone treatment corresponded to a decrease in the content of the key executive apoptotic protease, active caspase-3. In contrast to hydrocortisone, dexamethasone, a selective agonist of glucocorticoid receptors, did not induce any alterations in the expression of the studied proteins. Thus, hydrocortisone in vivo had an antiapoptotic effect on the expression of both forms of BDNF in the hippocampus of neonatal rats.