抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化及其意义的初步探讨

我们观察抑郁大鼠模型前额叶及海马区Rho激酶(ROCK)表达情况,仞步探讨Rho/ROCK通路在抑郁障碍形成中的作用.     

抑郁大鼠模型额叶及海马区Rho激酶表达变化的初步研究

目的：观察抑郁大鼠模型急性期额叶及海马区Rho激酶（ROCK）的表达变化,探讨Rho／ROCK通路是否与抑郁症形成有关。方法：建立Wistar大鼠抑郁症模型;在建模成功后24h迅速断头取前脑,在冰浴上分离出双侧前额叶及海马脑组织,应用Westernblot分别测定大鼠额叶及海马脑组织内ROCKⅠ及ROCKⅡ含量。结果：与正常对照组比,抑郁模型大鼠左侧和右侧前额叶ROCKⅠ表达均显著增高（分别P〈0．01,P〈0．05）,以左侧为著;ROCKⅡ表达亦有显著增高（均P〈0．05）。抑郁模型大鼠左右侧海马区域ROCKI表达显著增高（分NP〈0．05,P〈0．01）,以右侧明显;ROCKⅡ表达亦有显著增高（分别P〈0．05,P〈0．01）。结论：ROCKⅠ及ROCKⅡ可能参与了抑郁症形成的病理过程。     

MCAO模型大鼠海马区1β-HSD1的表达及活性变化

目的探讨大鼠海马区11β-羟类固醇脱氢酶1（11β-HSD1）在局灶性脑缺血再灌注过程中的表达及活性变化。方法采用大脑中动脉线栓法（MCAO）建立大鼠局灶性脑缺血-再灌注模型。42只雄性SD大鼠,随机分为脑缺血-再灌注后4、8、12、24、48、72h组和假手术组,每组6只。采用核糖核酸酶保护实验检测11β-HSD1mRNA的表达,采用Westernblot方法分析11β—HSD1蛋白表达水平变化,采用薄层层析（TLC）方法检测11β-HSD1酶活性。结果短暂性脑缺血-再灌注后大鼠海马区11β－HSD1表达增强,并于再灌注后24h达高峰,且11β-HSD1酶的活性也呈现类似变化规律。结论海马区11β—HSD1表达和活性的异常可能参与了大鼠脑缺血-再灌注损伤的病理生理过程。     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

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.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

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.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

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.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

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.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

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.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

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.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

目的 通过观察FeCl2皮层注射致损伤性癫痫(PTE)模型大鼠海马、额叶突触蛋白P38的表达变化.探讨突触可塑性在PTE发病机制中的作用. 方法 健康成年雄性SD大鼠采用随机数字表法分为正常对照组(n=5)、假手术组(n=12)、模型组(n=20).采取立体定向皮层注射FeCl2(0.1 moL/L,10μL)建立PTE模型,假手术组注入等量生理盐水,正常对照组不做处理.观察各组大鼠EEG的变化并应用免疫组织化学方法 检测大鼠造模后不同时间点(1 h、7 d、14 d、30 d)海马、额叶P38的表达. 结果大多数模型组大鼠在注射FeCl2后不久记录到癫痫样放电;与假手术组比较,模型组不同时间点右侧额叶P38表达减少.差异有统计学意义(P<0.05);与正常对照组和假手术组比较,致痫1h后,CA3区多形层、辐射层、腔隙层和齿状回(DG)分子层P38表达均无明显变化,7 d后P38表达增加,维持到30d,差异均有统计学意义(P<0.05). 结论 与突触蛋白P38表达相关的突触可塑性变化在PTE的发病机制中可能起重要作用.     

损伤性癫痫模型大鼠海马和额叶突触蛋白的动态表达

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.