Dynamic expressions of synapsin I and phosphorylated synapsin I in hippocampus of vascular dementia rats

AIM: To observe the dynamic changes of synapsin I expression and its phosphorylation in hippocampus in vascular dementia (VD) rats. METHODS: Eighty SD rats were randomly divided into sham-operated group (n=40) and VD model group (n=40), and the latter were established by repeatedly clipping the common carotid arteries with an intraperitoneal injection of sodium nitroprusside solution in anesthetized condition. The synaptic ultrastructural changes in hippocampal CA1 region and the expression levels of synapsinⅠ and phosphorylated synapsinⅠin hippocampus were observed by TEM and immunohistochemical staining method respectively in both sham-operated group and VD model group at 15 d, 1 month, 2 months and 4 months time points. RESULTS: No obviously pathological changes to CA1 area synapse were found in SO group. In model group rats, synaptic circa membrane ambiguity and fusion, synaptic circa membrane structure decreased the postsynaptic density, reduced synaptic vesicles and vesicle cluster. Above pathological changes became gradually severe along with the time prolongation after model-making operation. Compared with sham-operated group, the expression of synapsin I significantly reduced in CA1 region (P<0.01). However, no significant change in molecular layer of DG region (P>0.05) in model group was observed. The number of p-synapsin I positive neurons in DG and hippocampal CA1 region was less in model group than that in sham-operated group (P<0.05, P<0.01). The average absorbance values of p-synapsin I positive neurons in DG and hippocampal CA1 region in model group were decreased at 15 d and 1 month time points (P<0.01), but increased in CA1 region (P<0.01) and unchanged in DG at 2 months and 4 months time points (P>0.05). CONCLUSION: The damaged synaptic structure and depressed expression of synapsin I and its phosphorylation in presynaptic parts of hippocampus induced by repeatedly cerebral ischemia/reperfusion may contribute to the synaptic transmission disorders, especially the presynaptic disorder which may be one of the important pathogenesis of the initiation and development in vascular dementia rats.