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·kg⁻¹ alcohol treatment and   4 g·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.