In order to understand the alcohol's toxicity to the quantitative alternations of synapses in mouse visual cortex, the expression of synaptophysin after prenatal alcohol exposure was investigated. In present study, the experimental mice at P0, P7, P14 and P30 were grouped, as control, 2 g x kg(-1) alcohol treatment and 4 g x kg(-1) alcohol treatment. The pre-synaptic elements which were used to represent synapses were marked with synaptophysin (a synaptic vesicle associated protein) by immunocytochemistry technique. The synaptophysin positive boutons in layer VI of visual cortex were imaged under laser confocal microscope. With stereological methods, the number cal density of synapse in visual cortex was calculated in different groups at various ages. Moreover, Western blotting was carried out to detect the expression of synaptophysin in visual cortex. The results showed that prenatal alcohol exposure could cause synaptic loss with long-term effect and in a dose dependent manner. For instance, there were significant difference among the different treatment groups of P0, P14 and P30 as well (P < 0.05). Western blotting supported the results of immunofluorescent labeling. In conclusion, prenatal alcohol exposure can induce the synaptic loss dose dependently and with long-term effect. Our findings implicate that the synaptic loss with long-term effect in CNS probably contributes to the lifelong mental retardation and memorial lowliness associated with childhood FAS.

Objective To study the influence of miR-191 expression on the proliferation of human malignant meningioma cell line IOMM-Lee in vitro and to explore its mechanism.Methods The expression of miR-191 in malignant meningioma tissue,the adjacent normal tissues and human Malignant meningioma cell lines IOMM-Lee and CH157-MN was tested by Realtime PCR.miR-191 inhibitor was transfected in IOMM-Lee cells and MTT assay was employed to detect the cell viability.Bioinformatics prediction software was used in miR-191 target gene predictive analysis and verified by luciferase reporter system.The effect of EGR1 siRNA on the proliferation of IOMM-Lee cells was observed.Prorein interaction database was used to analyze which proteins could interact with EGR1.The effect of inhibition of EGR1 expression on TP53 protein expression was detected.The influence of inhibition of miR-191 expression on EGR1and TP53 expression was observed.Result The expression of miR-191 in malignant meningioma tissue (0.933±0.144) was higher than that in the adjacent normal tissue (0.459±0.104,P＜0.05).The expressiong of miR-191 in humam malignant meningioma cell line IOMM-Lee (1.25±0.07) was higher than that in CH157-MN cell line (0.50±0.14,P＜0.05).The cell proliferation capability was significantly decreased in miR-191 inhibitor group [(0.53±0.02) vs (0.74±0.01),P＜0.05].EGR1 was identified and validated to be a target gene of miR-191.Inhibition of EGR1 gene can promote OMM-Lee cell proliferation (0.83±0.02,0.71 ±0.01,P＜0.05).EGR 1 could positively regulate TP53 protein expression [(13 758.17±57.22) vs (10 239.00±71.30),P＜0.001.miR-191 Inhibition could increase EGR1 [(14 663.00±80.08) vs (11 184.33±153.90),P＜0.001] and TP53 expression [(15 206.17±102.08) vs(11 400.17±97.00),P＜0.001].Conclusion Downregulation of miR-191 can inhibit the proliferation of IOMM-Lee cell,which may be related to the upregulation of EGR1/TP53 signaling pathway.