Does maternal immune activation negatively affect fetal brain neuronal development?

母体免疫激活对胎儿脑神经发育的影响尚不清楚。我们研究了单链RNA多聚核糖肌苷酸-多聚核糖胞苷酸给药后母体免疫激活对幼年子代海马病理和突触功能的影响。Poly I：C处理组幼年子代海马CA 1区突触前肝齐射幅度和场兴奋性突触后电位斜率均显著低于对照组。此外，短突触可塑性，即配对脉冲易化率显着较高，长时程增强受损，海马CA 1区从青少年后代的聚IC处理的母鼠。与此相反，在海马组织学和神经元核抗原阳性细胞数从出生后后代的聚IC处理的母鼠没有影响。母体免疫激活导致海马突触功能障碍，但不是出生后神经元丢失。

Influence of maternal immune activation on neurodevelopment of fetal brain is not well understood. We investigated that influence of maternal immune activation by stranded RNA polyriboinosinic-polyribocytidilic acid administration on hippocampal pathology and synaptic function in juvenile offspring. In hippocampal CA1 region from juvenile offspring of Poly I:C treated dams, presynaptic fiver volley amplitude and field excitatory post synaptic potential slope were significant lower than control rats. In addition, short synaptic plasticity namely paired pulse facilitation ratio was significant higher and long-term potentiation impaired in hippocampal CA1 region from juvenile offspring of poly IC treated dams. In contrast, there were no effects in the hippocampal histology and neuronal nuclears antigen positive cell number from postnatal offspring of poly IC treated dams. Maternal immune activation causes of hippocampal synaptic dysfunction but not neuronal loss in the postnatal periods.