The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC 3052, Australia.
The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, VIC 3052, Australia; Department of Psychiatry, University of Melbourne, Parkville, VIC 3052, Australia.
Psychiatry Res. 2021 Jan;295:113564. doi: 10.1016/j.psychres.2020.113564. Epub 2020 Nov 7.
Environmental risk factors that operate at foetal or neonatal levels increase the vulnerability to schizophrenia, plausibly via stress-immune activation that perturbs the epidermal growth factor (EGF) system, a system critical for neurodevelopment. We investigated potential associations between environmental insults and immune and EGF system changes through a maternal immune activation (MIA) model, using the precocial spiny mice (Acomys cahirinus). After mid-gestation MIA prepubescent offspring showed elevated NF-κB1 protein in nucleus accumbens, decreased EGFR in caudate putamen and a trend for increased PI3K-110δ in ventral hippocampus. Thus, prenatal stress may cause a heightened NF-κB1-mediated immune attenuation of EGF system signalling.
环境风险因素在胎儿或新生儿期发挥作用会增加患精神分裂症的易感性，这可能是通过应激-免疫激活干扰表皮生长因子 (EGF) 系统来实现的，EGF 系统对于神经发育至关重要。我们通过母体免疫激活 (MIA) 模型研究了环境刺激与免疫和 EGF 系统变化之间的潜在关联，该模型使用早熟沙鼠 (Acomys cahirinus)。在妊娠中期 MIA 后，未成熟的后代在伏隔核中显示出 NF-κB1 蛋白升高，尾状核中 EGFR 降低，腹侧海马中 PI3K-110δ 升高。因此，产前应激可能导致 NF-κB1 介导的 EGF 系统信号免疫衰减增加。
