| 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 PO, P7, P14 and P30 were grouped, according to different treatments, such as control,2g/kg alcohol treatment and 4g/kg alcohol treatment as well. The pre-synaptic elements which were used to represent synapses were marked with synaptophysin (a synaptic vesicle associated protein) immunocytochemistry. 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 expressions of synaptophysin in visual cortex as well. Our results showed that alcohol prenatal exposure could cause synaptic loss with dose dependency and long-term effect. For instance, there were significant difference among the different treatment groups with dose dependency at PO, P14 and P30 as well (P＜0.05). Western blotting supported the results of immunofluorescent labeling as well. In conclusion, prenatal alcohol exposure can induce the synaptic loss with dose dependency and 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. |
