BACKGROUND： Previous studies have demonstrated that postsynaptic density protein-95 （PSD-95） is widely distributed in the central nervous system and is related to the development of the CNS and sensory signal trans...BACKGROUND： Previous studies have demonstrated that postsynaptic density protein-95 （PSD-95） is widely distributed in the central nervous system and is related to the development of the CNS and sensory signal transmission as well as acute or chronic nerve cell death following ischemic brain injury. OBJECTIVE： To semi-quantitatively determine the pathological changes of apoptotic facial neurons and the expression of PSD-95 in the facial nucleus following facial nerve injury of varying extents using immunohistochemical staining methods. DESIGN, TIME AND SETTING： Randomized, controlled animal experiments were performed in the Ultrasonic Institute of the Second Affiliated Hospital of Chongqing University of Medical Sciences from September to December 2007. MATERIALS： Sixty-five healthy, adult, Sprague-Dawley （SD） rats, both male and female, were used for this study. Rabbit anti-rat PSD-95 polyclonal antibody was purchased from Beijing Biosynthesis Biotechnology Co., Ltd. METHODS： SD rats were randomly assigned into a control group with five rats and three injured groups with 20 rats per group. Exposure, clamp and cut for bilateral facial nerve trunks were performed in the rats of the injury groups, and no injury was inflicted on the rats of the control group. MAIN OUTCOME MEASURES; The brainstems of all the rats were excised on days 1, 3, 7, and 14 post injury, and then the facial nuclei were stained with hematoxylin-eosin to observe any pathological changes due to apoptosis in facial neurons. PSD-95 expression in facial nuclei was detected by immunohistochemistry and the number of PSD-95 positive cells was counted under a light microscope. RESULTS： The expression of PSD-95 in the facial nucleus and morphology of the facial neuron within the exposure group had no obvious changes at various points in time tested （P 〉 0.05）. However, the expressions of PSD-95 in the facial nucleus of the clamp group and cut group increased on day 1 post injury （P 〈 0.05）, and showed further increase on day 7 post injury （P 〈 0.01 ）. This did not decrease until day 14 post injury. Facial neuron apoptosis was detected on day 3 post injury and this was even more obvious on day 7 and was maintained to day 14 post injury. The number of cells expressing PSD-95 and displaying severe degrees of facial neuron apoptosis were as follows： cut group 〉 clamp group 〉 exposure group. CONCLUSION： The apoptotic extent of facial neurons and the expression of PSD-95 in apoptotic facial neurons increased with the degree of aggravation of injured severity of facial nerve.展开更多
Postsynaptic density protein-95 and synaptophysin participate in synaptic reorganization in the forebrain of epilepsy models. However, the time-effect relationship between dynamic synapsin expression in hippocampus an...Postsynaptic density protein-95 and synaptophysin participate in synaptic reorganization in the forebrain of epilepsy models. However, the time-effect relationship between dynamic synapsin expression in hippocampus and synaptic reorganization in the post-traumatic epilepsy model remains unclear. FeCI2 was injected into the hippocampal CA3 region of the right forebrain in rats to induce post-traumatic epilepsy. Postsynaptic density protein-95 and synaptophysin expression was detected using immunohistochemistry. Epileptiform discharge induced by FeCI2 injection was determined in rat forebrain neurons, revealing decreased postsynaptic density protein-95 expression at 24 hours and lowest levels at 7 days. Synaptophysin expression was markedly reduced at 24 hours, but increased at 7 days. Postsynaptic density protein-95 and synaptophysin expression was consistent with abnormal mossy fiber sprouting and synaptic reorganization following neuronal injury in the hippocampal CA3 region of FeCI2-induced epilepsy models.展开更多
目的观察小鼠学习记忆能力及其海马区突触功能相关蛋白脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)、突触后致密蛋白95(postsynaptic density protein 95,PSD95)及GluA1表达的增龄性变化。方法观察10周龄(青年组)和21...目的观察小鼠学习记忆能力及其海马区突触功能相关蛋白脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)、突触后致密蛋白95(postsynaptic density protein 95,PSD95)及GluA1表达的增龄性变化。方法观察10周龄(青年组)和21月龄(老年组)C57BL/6雄性小鼠Morris水迷宫训练和测试表现,并应用Western blot技术检测两组小鼠海马区BDNF、PSD95、GluA1的蛋白表达。结果与青年组相比,老年组小鼠水迷宫测试中的学习记忆能力明显下降(P均<0.05),其海马区总蛋白BDNF、PSD95、GluA1的表达量均显著下降(P均<0.05),海马区膜蛋白GluA1的表达量也明显下降(P<0.05)。结论老年小鼠学习记忆能力下降伴随着海马区突触功能相关蛋白BDNF、PSD95、GluA1表达的一致下降。展开更多
目的:探讨静脉用低剂量米诺环素对局灶性脑缺血再灌注大鼠认知功能障碍及缺血侧海马生长相关蛋白-43(growth associated protein-43,GAP-43)和突触后致密物质-95(postsynaptic density 95,PSD-95)表达的影响。方法:采用线栓法建立Spragu...目的:探讨静脉用低剂量米诺环素对局灶性脑缺血再灌注大鼠认知功能障碍及缺血侧海马生长相关蛋白-43(growth associated protein-43,GAP-43)和突触后致密物质-95(postsynaptic density 95,PSD-95)表达的影响。方法:采用线栓法建立Sprague-Dawley大鼠大脑中动脉阻塞再灌注模型,将45只雄性大鼠随机分为假手术组、模型组及米诺环素组(n=15)。分别采用免疫组织化学及免疫印迹法检测术后2周大鼠缺血侧海马GAP-43和PSD-95蛋白的表达,Morris水迷宫实验评价大鼠的行为学改变。结果:同假手术组相比,模型组大鼠缺血侧海马GAP-43(0.49±0.03)和PSD-95(0.92±0.04)表达明显增高(P=0.000);大鼠逃避潜伏期明显延长[(44.2±10.0)s],穿过原平台次数(2.6±0.9)和在目标象限探索时间百分率明显降低[(19.2±2.1)%,P=0.000)]。同模型组相比,尾静脉给予3 mg/kg米诺环素治疗后,大鼠缺血侧海马GAP-43(0.72±0.05)表达明显增加,PSD-95表达降低(0.67±0.05,P=0.000),大鼠逃避潜伏期明显缩短[(30.8±7.6)s,P=0.020]、穿过原平台次数(4.4±1.1,P=0.012)和在目标象限探索时间百分率明显增加[(30.4±2.7)%,P=0.000)]。结论:低剂量米诺环素能显著改善脑缺血再灌注后大鼠学习记忆能力,其机制可能与上调GAP-43和下调PSD-95表达有关。展开更多
目的探讨戊四氮点燃癫痫对大鼠空间学习记忆的影响及可能的分子机制。方法戊四氮(pentylenetet-razol,PTZ)点燃建立慢性癫痫(chronic epileptic,CEP)模型,Morris水迷宫进行行为学检测,免疫组织化学方法观察大鼠海马CA1、CA3区突触素(syn...目的探讨戊四氮点燃癫痫对大鼠空间学习记忆的影响及可能的分子机制。方法戊四氮(pentylenetet-razol,PTZ)点燃建立慢性癫痫(chronic epileptic,CEP)模型,Morris水迷宫进行行为学检测,免疫组织化学方法观察大鼠海马CA1、CA3区突触素(synaptophysin,P38)和突触后致密物95(postsynaptic density 95,PSD-95)的表达,并用计算机图像分析系统对免疫反应结果进行处理。结果水迷宫试验检测癫痫组大鼠空间学习记忆能力受损;免疫组化结果表明其海马CA1、CA3区P38和PSD-95免疫反应产物较对照组明显减少(P<0.01,P<0.05)。结论戊四氮点燃癫痫大鼠伴有学习记忆功能减退,其海马神经元P38和PSD-95的表达减少可能参与了空间学习记忆受损。展开更多
文摘BACKGROUND： Previous studies have demonstrated that postsynaptic density protein-95 （PSD-95） is widely distributed in the central nervous system and is related to the development of the CNS and sensory signal transmission as well as acute or chronic nerve cell death following ischemic brain injury. OBJECTIVE： To semi-quantitatively determine the pathological changes of apoptotic facial neurons and the expression of PSD-95 in the facial nucleus following facial nerve injury of varying extents using immunohistochemical staining methods. DESIGN, TIME AND SETTING： Randomized, controlled animal experiments were performed in the Ultrasonic Institute of the Second Affiliated Hospital of Chongqing University of Medical Sciences from September to December 2007. MATERIALS： Sixty-five healthy, adult, Sprague-Dawley （SD） rats, both male and female, were used for this study. Rabbit anti-rat PSD-95 polyclonal antibody was purchased from Beijing Biosynthesis Biotechnology Co., Ltd. METHODS： SD rats were randomly assigned into a control group with five rats and three injured groups with 20 rats per group. Exposure, clamp and cut for bilateral facial nerve trunks were performed in the rats of the injury groups, and no injury was inflicted on the rats of the control group. MAIN OUTCOME MEASURES; The brainstems of all the rats were excised on days 1, 3, 7, and 14 post injury, and then the facial nuclei were stained with hematoxylin-eosin to observe any pathological changes due to apoptosis in facial neurons. PSD-95 expression in facial nuclei was detected by immunohistochemistry and the number of PSD-95 positive cells was counted under a light microscope. RESULTS： The expression of PSD-95 in the facial nucleus and morphology of the facial neuron within the exposure group had no obvious changes at various points in time tested （P 〉 0.05）. However, the expressions of PSD-95 in the facial nucleus of the clamp group and cut group increased on day 1 post injury （P 〈 0.05）, and showed further increase on day 7 post injury （P 〈 0.01 ）. This did not decrease until day 14 post injury. Facial neuron apoptosis was detected on day 3 post injury and this was even more obvious on day 7 and was maintained to day 14 post injury. The number of cells expressing PSD-95 and displaying severe degrees of facial neuron apoptosis were as follows： cut group 〉 clamp group 〉 exposure group. CONCLUSION： The apoptotic extent of facial neurons and the expression of PSD-95 in apoptotic facial neurons increased with the degree of aggravation of injured severity of facial nerve.
基金the General Program of Department of Education of Guangxi Zhuang Autonomous Region,No.Guijiaokeyan[2007]34
文摘Postsynaptic density protein-95 and synaptophysin participate in synaptic reorganization in the forebrain of epilepsy models. However, the time-effect relationship between dynamic synapsin expression in hippocampus and synaptic reorganization in the post-traumatic epilepsy model remains unclear. FeCI2 was injected into the hippocampal CA3 region of the right forebrain in rats to induce post-traumatic epilepsy. Postsynaptic density protein-95 and synaptophysin expression was detected using immunohistochemistry. Epileptiform discharge induced by FeCI2 injection was determined in rat forebrain neurons, revealing decreased postsynaptic density protein-95 expression at 24 hours and lowest levels at 7 days. Synaptophysin expression was markedly reduced at 24 hours, but increased at 7 days. Postsynaptic density protein-95 and synaptophysin expression was consistent with abnormal mossy fiber sprouting and synaptic reorganization following neuronal injury in the hippocampal CA3 region of FeCI2-induced epilepsy models.
文摘目的观察小鼠学习记忆能力及其海马区突触功能相关蛋白脑源性神经营养因子(brain-derived neurotrophic factor,BDNF)、突触后致密蛋白95(postsynaptic density protein 95,PSD95)及GluA1表达的增龄性变化。方法观察10周龄(青年组)和21月龄(老年组)C57BL/6雄性小鼠Morris水迷宫训练和测试表现,并应用Western blot技术检测两组小鼠海马区BDNF、PSD95、GluA1的蛋白表达。结果与青年组相比,老年组小鼠水迷宫测试中的学习记忆能力明显下降(P均<0.05),其海马区总蛋白BDNF、PSD95、GluA1的表达量均显著下降(P均<0.05),海马区膜蛋白GluA1的表达量也明显下降(P<0.05)。结论老年小鼠学习记忆能力下降伴随着海马区突触功能相关蛋白BDNF、PSD95、GluA1表达的一致下降。
文摘目的探讨戊四氮点燃癫痫对大鼠空间学习记忆的影响及可能的分子机制。方法戊四氮(pentylenetet-razol,PTZ)点燃建立慢性癫痫(chronic epileptic,CEP)模型,Morris水迷宫进行行为学检测,免疫组织化学方法观察大鼠海马CA1、CA3区突触素(synaptophysin,P38)和突触后致密物95(postsynaptic density 95,PSD-95)的表达,并用计算机图像分析系统对免疫反应结果进行处理。结果水迷宫试验检测癫痫组大鼠空间学习记忆能力受损;免疫组化结果表明其海马CA1、CA3区P38和PSD-95免疫反应产物较对照组明显减少(P<0.01,P<0.05)。结论戊四氮点燃癫痫大鼠伴有学习记忆功能减退,其海马神经元P38和PSD-95的表达减少可能参与了空间学习记忆受损。
