匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

Objective To investigate the roles of somatostatin(SS)positive intemeurons in the development and compensation of temporal lobe epilepsy.Methods Piloearpine-induced epilepsy rat model was established.Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive intemeurons in different domains of the hippocampus at difierent time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluorescence staining with SS and Fluoro-Jade B(FJB)at 7 and 60 days after status epilepticus (SE).Results In the exoerimental rat group,the number of SS positive neurons decreased in each hippocampal domain,and it reached the lowest at 7 days post-SE(There were 11.1±3.3 in hilus,2.8±0.9 in CA1region and 1.8±0.7 in CA1region,t=13.519,9.644 and 8.808,all P<0.01).In chronic phase,the number of SS neurons gradually recovered,and exceeded the control group in CA1 area at 60 days post-SE(12.8±1.5 vs 8.8±1.3,t=-4.506,P<0.01),however,the number of SS neurons in the hilus(25.5±4.6)and CA1 area(4.8±0.8)remained significantly less than normal levels(t value were 4.691 and 3.953.both P<0.01).Increased SS positive fibers were found in the lacunosum-molecular (1m)layer and outer molecular layer of dentate gyrus after 30 days post-SE,and numerous SS positive fibers were seen threnghout the layers of area CA1 at 60 days post-SE.Double immunofluuorescence revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE.Conclusions SS intemeurons loss plays an important role in the development of temporal lobe epilepsy.The loss is partially caIlsed by the degeneration and death of neurons;SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.     

匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

Objective To investigate the roles of somatostatin(SS)positive intemeurons in the development and compensation of temporal lobe epilepsy.Methods Piloearpine-induced epilepsy rat model was established.Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive intemeurons in different domains of the hippocampus at difierent time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluorescence staining with SS and Fluoro-Jade B(FJB)at 7 and 60 days after status epilepticus (SE).Results In the exoerimental rat group,the number of SS positive neurons decreased in each hippocampal domain,and it reached the lowest at 7 days post-SE(There were 11.1±3.3 in hilus,2.8±0.9 in CA1region and 1.8±0.7 in CA1region,t=13.519,9.644 and 8.808,all P<0.01).In chronic phase,the number of SS neurons gradually recovered,and exceeded the control group in CA1 area at 60 days post-SE(12.8±1.5 vs 8.8±1.3,t=-4.506,P<0.01),however,the number of SS neurons in the hilus(25.5±4.6)and CA1 area(4.8±0.8)remained significantly less than normal levels(t value were 4.691 and 3.953.both P<0.01).Increased SS positive fibers were found in the lacunosum-molecular (1m)layer and outer molecular layer of dentate gyrus after 30 days post-SE,and numerous SS positive fibers were seen threnghout the layers of area CA1 at 60 days post-SE.Double immunofluuorescence revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE.Conclusions SS intemeurons loss plays an important role in the development of temporal lobe epilepsy.The loss is partially caIlsed by the degeneration and death of neurons;SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.     

神经生长因子促血管生成与神经再生的相关性研究

[目的]研究在大鼠脑缺血模型中,通过阻断粘着斑激酶(FAK)磷酸化,来抑制神经生长因子(NGF)的促血管生成作用,从而观察其对NGF促神经再生作用的影响,探讨NGF促血管生成作用和促神经再生二者的关系.[方法]雄性SD大鼠24只,随机分为四组:假手术组、脑缺血组、NGF治疗组、NGF+ TAE226(FAK抑制剂)干预组,制备大鼠局灶性永久性脑缺血模型并干预,术后d14取室管膜下区(SVZ)和海马齿状回区(SGZ)脑组织做组织切片,用荧光标记法,统计细胞增殖标记物,Brdu以及SVZ区和SGZ区神经元前体细胞标记蛋白,DCX蛋白的表达,观察神经干细胞向神经元分化的情况.[结果]假手术组和脑缺血组少见Brdu的标记阳性细胞,SVZ和SGZ区少有DCX蛋白表达;NGF组Brdu标记的阳性细胞及SVZ和SGZ区DCX蛋白表达均明显多于其他三组;NGF+ TAE226组较NGF组双标的阳性神经元数目均有较明显下降,但多于脑缺血组,且差异有显著性(P＜0.05).[结论]大鼠脑缺血后,NGF的促血管生成作用有利于缺血后神经再生.     

神经病学临床教学中的多媒体优化组合

通过多媒体技术在神经病学临床教学中的探索和总结，指出多媒体网络在神经内科临床教学中的优势和前景。     

匹罗卡品致(癎)大鼠海马中表达生长抑素的中间神经元数目变化及其轴突出芽

Objective To investigate the roles of somatostatin(SS)positive intemeurons in the development and compensation of temporal lobe epilepsy.Methods Piloearpine-induced epilepsy rat model was established.Immunohistochemistry method was used to detect number changes and axonal sprouting of SS positive intemeurons in different domains of the hippocampus at difierent time points.Degeneration of SS positive interneurons and their neurophils were detected by the double immunofluorescence staining with SS and Fluoro-Jade B(FJB)at 7 and 60 days after status epilepticus (SE).Results In the exoerimental rat group,the number of SS positive neurons decreased in each hippocampal domain,and it reached the lowest at 7 days post-SE(There were 11.1±3.3 in hilus,2.8±0.9 in CA1region and 1.8±0.7 in CA1region,t=13.519,9.644 and 8.808,all P<0.01).In chronic phase,the number of SS neurons gradually recovered,and exceeded the control group in CA1 area at 60 days post-SE(12.8±1.5 vs 8.8±1.3,t=-4.506,P<0.01),however,the number of SS neurons in the hilus(25.5±4.6)and CA1 area(4.8±0.8)remained significantly less than normal levels(t value were 4.691 and 3.953.both P<0.01).Increased SS positive fibers were found in the lacunosum-molecular (1m)layer and outer molecular layer of dentate gyrus after 30 days post-SE,and numerous SS positive fibers were seen threnghout the layers of area CA1 at 60 days post-SE.Double immunofluuorescence revealed that a few SS positive interneurons and fibers were also labeled by FJB in area CA1 at 7 days post-SE and in CA domain/hilus at 60 days post-SE.Conclusions SS intemeurons loss plays an important role in the development of temporal lobe epilepsy.The loss is partially caIlsed by the degeneration and death of neurons;SS positive neurophils increase within area CA1 in chronic phase may play a significant role in the generation and compensation of temporal lobe epilepsy.     

脱髓鞘脑病的临床特点分析

目的:探讨脱髓鞘脑病的临床特点。方法:回顾性分析50例脱髓鞘脑病患者的临床表现、病理检查结果、实验室和影像学资料及治疗。结果:50例患者的临床表现多样,主要为精神异常、运动障碍和视力损害,MRI检查有脑内广泛长T1、长T2异常信号改变,病理活检可见白质脱髓鞘改变。结论:脱髓鞘脑病临床表现复杂多样,诊断需结合患者的年龄、病程、前驱病史、临床症状、中枢神经系统病灶的数目和分布、实验室、影像学检查和病理活检,明确诊断后应尽早治疗。     

Brugada综合征误诊为癫痫一例

患者 男,40岁,因"发作性晕厥十余年,加重1 d"于2010年7月7日住进湘雅医院神经内科.患者十余年前开始出现反复晕厥,发作前感上腹部不适,继而迅速出现黑朦,并晕厥倒地.发病时面色苍白,口唇发绀,大汗淋漓,牙关紧闭,肌张力高,双肘关节屈曲,无口吐白沫、四肢抽搐及大小便失禁,每次持续约1～2min,清醒后感四肢乏力、心慌,无头痛头晕,大约每2～12个月发作一次,并曾摔伤过头部.3年前神经内科门诊首诊,拟诊"癫痫".患者间隔2年后再发晕厥2次,入院前1 d再次晕厥5次,发作情况同前.家族中患者哥哥有夜间睡眠时猝死史,3兄妹有过类似晕厥发作史.     

亨廷顿蛋白相关蛋白1与脑源性神经营养因子的胞吞关系的机制研究

目的探讨亨廷顿蛋白相关蛋白1(HAP1)与脑源性神经营养因子(mBDNF)胞吞的相关性和可能的机制。方法神经营养因子(NGF)诱导分化PC 1 2细胞,将荧光质粒HAP1A-CFP和(或)mBDNF-ds-red转染进入细胞,培养4 8 h后在含有BDNF或p7 5NTR抗体的培养基中继续培养,激光共聚焦显微镜观察荧光的表达情况及其在细胞中的定位;利用小鼠皮层神经元(正常型和HAP1基因敲除型)在生物素标记mBDNF的培养基中孵育6 0 m in,激光共聚焦显微镜观察皮层神经元免疫荧光的效果。结果共转染HAP1A-CFP和mBDNF-ds-red质粒的细胞,2种荧光蛋白存在部分共定位3 4%。共转染的细胞在抗BDNF培养基孵育下,或者单转染HAP1A-CFP质粒的细胞在mBDNF-ds-red荧光蛋白+抗BD-NF/抗p7 5NTR培养基孵育下,2种荧光蛋白几乎没有共定位现象。单转染HAP1A-CFP质粒的细胞在mBDNF-ds-red荧光蛋白培养基孵育下,mBDNF与HAP1蛋白的共定位比例高达9 3%。正常新生小鼠皮层神经元内可见内吞的mBDNF免疫荧光,HAP1基因敲除小鼠的皮层神经元内未见。结论 mBDNF的胞吞必需HAP1的表达和参与。     

匹罗卡品致痫大鼠海马神经肽Y中间神经元数目变化及其轴突出芽

目的:探讨神经肽Y(neuropeptide Y,NPY)中间神经元在颞叶癫痫的发生和自我修复中的作用.方法:建立匹罗卡品致痫模型,应用免疫组织化学技术动态观察大鼠海马NPY中间神经元的数目变化及其轴突出芽.结果:实验组大鼠腹腔注射氯化锂-匹罗卡品后,癫痫持续状态(status epilepticus, SE)诱发成功率为92.9%,死亡率19.2%.免疫组织化学结果显示,实验组大鼠海马门区NPY中间神经元数目在SE后下降,至7 d时降至最低(P<0.01),慢性期开始恢复,SE后60 d时NPY神经元数目与对照组相比仍有减少(P<0.05);CA区域除SE后7 d CA3区NPY神经元数目稍减少外(P<0.05),其余时间点均无明显变化(P>0.05);SE后30 d齿状回分子层可见增多的NPY阳性纤维.结论:NPY中间神经元在不同部位不同时段对颞叶癫痫所致损伤的敏感性不同,NPY中间神经元的缺失在颞叶癫痫发生中起重要作用,NPY中间神经元的轴突出芽在颞叶癫痫的自我修复中起作用.