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首页> 外文期刊>Neurobiology of learning and memory >Postnatal exposure to poly (I:C) impairs learning and memory through changes in synaptic plasticity gene expression in developing rat brain
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Postnatal exposure to poly (I:C) impairs learning and memory through changes in synaptic plasticity gene expression in developing rat brain

机译：产后暴露于聚（i：c）通过发展大鼠脑中的突触塑性基因表达的变化损害学习和记忆

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Viral infection during early stage of life influences brain development and results in several neurodevelopmental disorders such as schizophrenia, autism and behavioral abnormalities. However, the mechanism through which infection causes long-term behavioral defects is not well known. To elucidate this, we have used synthetic polyinosinic-polycytidylic acid [poly (I:C)) which acts as a dsRNA molecule and interacts with toll-like receptor 3 (TLR-3) of microglia cells to evoke the immune system, thus mimicking the viral infection. Rat pups of postnatal day (PND) 7 were infused with a single dose of poly (I:C) (5 mg/kg BW) and vehicle alone to controls. When these pups grew to 3, 6 and 12 weeks, their spatial and fear conditioning memory were impaired as assessed by Morris water maze and passive avoidance test, respectively. We checked the immune activation by staining of TNF-alpha in the hippocampus and observed that poly (I:C) exposure elevated the number of TNF-alpha positive cells immediately after 12 h of infusion in one week rat and it persisted up to postnatal age of 3 and 12 weeks. Moreover, poly (I:C) significantly decreased the binding of H-3-QNB to the cholinergic receptors in the frontal cortex and hippocampus of 3 and 6 weeks rats as compared to control but did not change significantly in 12 weeks rats. RT-PCR and immunoblotting results showed that poly (I:C) exposure upregulated the expression of memory associated genes (BDNF, Arc, EGR1) at mRNA and protein level in frontal cortex and hippocampus of 3 weeks rats as compared to control. However, long-time persistence of poly (I:C) effects significantly decreased the expression of these genes in both brain regions of 12 weeks rats. Taken together, it is evident that early life exposure to poly (I:C) has a long-term effect and impairs learning and memory, probably through TNF-a mediated neuroinflammation and alteration in the expression of memory associated genes in frontal cortex and hippocampus of rats.
机译：寿命早期病毒感染影响脑发育，导致几种神经发育障碍，如精神分裂症，自闭症和行为异常。然而，感染引起长期行为缺陷的机制并不众所周知。为了阐明这一点，我们使用了合成多胞聚氰基 - 聚环酸[聚（i：c）），其充当DsRNA分子，与Microglia细胞的Toll样受体3（TLR-3）相互作用以引起免疫系统，从而模仿病毒感染。产后后天（PND）7的幼鼠用单剂量的聚（I：C）（5mg / kg Bw）和单独进行对照的载体进行注入。当这些幼崽增长到3例，6和12周，他们的空间和恐惧调理记忆分别被莫里斯水迷宫和被动避免试验评估损害。通过在海马中染色TNF-α进行染色，观察到聚（I：c）曝光在一周大鼠输液12小时后立即升高TNF-α阳性细胞的数量，它持续到产后后期3和12周。此外，与对照相比，聚（I：C）显着降低了H-3-QNB在3和6周大鼠的胆碱能受体中的结合，但在12周大鼠中没有显着变化。 RT-PCR和免疫印迹结果表明，与对照相比，聚（I：C）曝光上调了前部皮层和海马的MRNA和蛋白质水平的记忆相关基因（BDNF，弧，EGR1）的表达。然而，聚（i：c）效应的长期持久性显着降低了12周大鼠大脑区域中这些基因的表达。显而易见的是，早期生命暴露于聚（i：c）具有长期效果和损害学习和记忆，可能是通过TNF-A介导的神经炎症和反应在额叶和海马中的记忆相关基因的表达中的改变大鼠。

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