Time course of cortical and hippocampal synaptophysin expression changes in rats with posttraumatic epilepsy induced by intracortical FeCl2 injection
10.3760/cma.j.issn.1671-8925.2009.06.003
- VernacularTitle:损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达
- Author:
Yuan-Xiang LIN
1
;
Ru-Xiang XU
;
Xiao-Dan JIANG
;
De-zhi NG KA
;
Yi-Quan KE
;
Mou-Xuan DU
;
Li-Shnang XU
Author Information
1. 福建医科大学附属第一医院
- Keywords:
Posttraumatic Epilepsy;
Ferrous chloride;
Synaptophysin;
Synaptic plasticity
- From:
Chinese Journal of Neuromedicine
2009;8(6):551-555
- CountryChina
- Language:Chinese
-
Abstract:
Objective To observe the time course of changes in synaptophysin (P38) expression in the cortex and hippocampus of rats with posttraumatic epilepsy (PTE), and explore the role of synaptic plasticity in the epileptogenesis of PTE. Methods Thirty-seven male Sprague-Dawley rats were randomized into normal control group (n=5), sham-operated group (n=12) with intracortical saline injection, and PTE model group (n=20) with stereotactic FeCl<,2> injection (0.1 mol/L, 10 μ1) into the motor cortex. The expression of P38 in the brain cortex and hippocampus of the rats was detected immunohistochemically at 1 h and 7, 14 and 30 days after the injections. Results Most of the rats with FeCl<,2> injection developed isolated epileptiform discharges soon alter the injection. Compared with the sham-operated groups, the rats in PTE group showed significantly decreased P38 expression in the right frontal cortex at all the time points of measurement (P<0.05). At 1 h after FeCl<,2> injection, P38 expression in the polymorphic layer, stratum lacunosum and stratum radiatum of the right hippocampai CA3 area and DG molecular layer underwent no significant changes (P>05), but at 7 days, the expression increased significantly in all the stratum regions of the right hippocampal CA3 area, and this high expression level was maintained till 30 days after the injection. Conclusion Synaptic plasticity alterations in relation to P38 expression changes in the cortex and hippocampus may play an important role in the epileptogenesis of PTE in this rat model.
