MgSO₄ has been used for the past two decades as neuroprotective treatment in a variety of preterm conditions. Despite the putative advantages of MgSO₄ as a neuroprotective agent in the preterm brain, the short- and long-term molecular function of MgSO₄ as a neuroprotective agent has not been fully elucidated. Neuregulin (NRG1)-ErbB4 signaling plays a critical role in embryonic brain development, in the biology of dopaminergic, GABAergic, and glutamatergic systems. We hypothesize that this pathway may be associated with the neuroprotective role of MgSO₄. The current study aims to investigate the ability of MgSO₄ to modulate the normal developing expression pattern of selected genes related to the NRG1-ErbB, dopaminergic, GABAergic, and glutamatergic systems. We demonstrate that overall short-term treatment of dam rats with MgSO₄ affects the expression of fetal brain NRG1, NRG3, ErbB4, GAD67, tyrosine hydroxylase (TH), dopamine D₂ and D₁ receptors, GluN1, and GluN2B. More specifically, the administration of MgSO₄ alters the expression of NRG-ErbB, GAD67, TH, and D2R at early gestation day 16 (GD16) regardless of the activation of the maternal immune system by lipopolysaccharide (LPS). Our data suggest that MgSO₄ treatment may affect the expression of major neuronal systems and pathways mostly at an early gestation day. These changes might be an initial clue (foundation stone) in the molecular mechanism that underlies the beneficial effect of MgSO₄ as a neuroprotective agent for the developmental brain.

过去二十年来，MgSO ₄一直被用作各种早产疾病的神经保护治疗。尽管 MgSO ₄作为早产儿大脑中的神经保护剂具有公认的优势，但尚未完全阐明MgSO ₄作为神经保护剂的短期和长期分子功能。神经调节蛋白 (NRG1)-ErbB4 信号传导在胚胎大脑发育、多巴胺能、GABA 能和谷氨酸能系统的生物学中起着关键作用。我们假设该通路可能与 MgSO ₄的神经保护作用有关。目前的研究旨在调查 MgSO ₄的能力调节与 NRG1-ErbB、多巴胺能、GABA 能和谷氨酸能系统相关的选定基因的正常发育表达模式。我们证明，用 MgSO ₄对大坝大鼠进行整体短期治疗会影响胎儿大脑 NRG1、NRG3、ErbB4、GAD67、酪氨酸羟化酶 (TH)、多巴胺 D ₂和 D ₁受体、GluN1 和 GluN2B 的表达。更具体地说，无论母体免疫系统是否被脂多糖 (LPS) 激活，MgSO ₄的给药都会改变 NRG-ErbB、GAD67、TH 和 D2R 在妊娠早期第 16 天 (GD16) 的表达。我们的数据表明 MgSO ₄治疗可能主要在妊娠早期影响主要神经元系统和通路的表达。这些变化可能是分子机制中的一个初步线索（基石），它是 MgSO ₄作为发育大脑的神经保护剂的有益作用的基础。