Abstract—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.

中文翻译：

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地塞米松给药后新生大鼠海马神经营养因子3的表达

摘要-围产期个体发育期间糖皮质激素水平升高可能会引起神经病理学的进一步发展，其机制可能涉及神经营养素表达受损引起的脑细胞凋亡，包括实际上未被研究的神经营养因子3（NT3）。为了澄清这个问题，我们探讨了糖皮质激素地塞米松（DEX）对NT3和关键凋亡凋亡蛋白酶caspase-3，mRNA水平以及未成熟（proNT3）和成熟（matNT3）形式的神经营养蛋白的影响。服用DEX后6或24小时，对3–4日龄大鼠的海马区。在6小时而不是24小时内，DEX增加了整个海马中NT3 mRNA的水平，proNT3和matNT3蛋白也包含了CA1-3区和该结构的齿状回。在这种情况下，凋亡性proNT3的表达暂时超过matNT3；然而，这并没有伴随caspase-3 mRNA水平的增加。