Mg^2＋对小鼠学习记忆的影响及其与海马CA3区和大脑皮层突触界面结？…

采用行为测试和亚微结构定量分析相结合的方法，研究了Ｍｇ＾２＋对小鼠分辨学习和记忆巩固的影响，同时测定了海马ＣＡ３区及大脑皮层突触界面结构的变化，实验结果表明，慢性给予Ｍｇ＾２＋后，血浆及海马内Ｍｇ＾２＋含量有一定的程度的升高，小鼠分辨学习能力显著下降，记忆巩固受到破坏，并且海马ＣＡ３区及大脑皮层的突触后致密物质（ｐｏｓｔ－ｓｙｎａｐｔｉｃｄｅｎｓｉｔｙ，ＰＳＤ）显著变薄，同时，皮层突触活性区长度亦     

Mg~(2 )对小鼠学习记忆的影响及其与海马CA_3区和大脑皮层突触界面结构的相关性

采用行为测试和亚微结构定量分析相结合的方法，研究了Ｍｇ２＋对小鼠分辨学习和记忆巩固的影响，同时测定了海马ＣＡ３区及大脑皮层突触界面结构参数的变化。实验结果表明：慢性给予Ｍｇ２＋后，血浆及海马内Ｍｇ２＋含量有一定程度的升高，小鼠分辨学习能力显著下降，记忆巩固受到破坏，并且海马ＣＡ３区及大脑皮层的突触后致密物质（ｐｏｓｔ—ｓｙｎａｐｔｉｃｄｅｎｓｉｔｙ，ＰＳＤ）显著变薄，同时，皮层突触活性区长度亦显著缩短。以上结果提示，脑内Ｍｇ２＋水平过高造成的学习记忆过程损伤可能与其改变ＰＳＤ厚度和突触活性区长度密切相关。     

脑缺血选择性海马CA1区神经元损害的实验研究

采用Ｐｕｌｓｉｎｅｌｉ－Ｂｒｉｅｒｌｅｙ４血管阻塞脑缺血模型观察了大鼠全脑缺血２０ｍｉｎ再灌流８ｈ，ｃ－ｆｏｓ基因表达及再灌流７ｄ海马ＣＡ１区迟发性神经元损害。在缺血再灌流早期（８ｈ）海马ＣＡ１区极少ｃ－ｆｏｓ表达，而齿状回、海马ＣＡ３区、杏仁核大量ｃ－ｆｏｓ表达。缺血再灌流晚期（７ｄ）镀银染色显示海马ＣＡ１区神经元及其突触终末带呈黑色溃变相，而齿状回、海马ＣＡ３区、杏仁核呈金黄色正常相。相邻切片ＨＥ染色示缺血组海马ＣＡ１区核完整的锥体细胞数（５±２．６个／２００μｍ）与对照组（４０±２．９个／μｍ）比较差异有显著意义（Ｐ＜０．０１）。脑缺血诱导的ｃ－ｆｏｓ基因表达对于缺血易损海马ＣＡ１区迟发性神经元坏死可能起直接的调控作用。     

醒脑健神胶囊对SHRsp出血性中风海马EAA和神经元的影响

本实验采用卒中易感型自发性高血压大鼠（ＳＨＲｓｐ），观察醒脑健神胶囊对出血性中风海马区兴奋性氨基酸（ＥＡＡ）和ＣＡ１区神经元的影响。结果发现：病理组海马区谷氨酸（Ｇｌｕ）和天门冬氨酸（Ａｓｐ）含量明显升高，治疗组能显著降低出血性中风海马区Ｇｌｕ和Ａｓｐ的含量（Ｐ＜０．０５）。病理形态观察，治疗组ＣＡ１区神经元损伤轻，细胞计数与病理组相比显著升高（Ｐ＜０．０１）；电镜亦显示：治疗组能使出血性中风造成的脑组织水肿、变性和坏死得到明显改善。研究结果提示，醒脑健神胶囊可能是通过降低ＥＡＡ的含量起到保护神经细胞作用     

小鼠衰老性记忆障碍的脑内突触形态学变化

本文定且研究了小鼠的海马CA3区和大脑皮层感觉运动区GrayⅠ型突触界面结构。衰老小鼠按一次性被动回避反应检测结果分成记忆宪好组和记忆衰退组，两组的统计比较结果表明：记忆衰退组突触后致密物质厚度极显著变小（在海马，P＜0．01；在皮层，P＜0．001）；海马CA3区突触活性带长度极显著变短（P＜0．01）；而上述两脑区突触间隙宽度则极显著增大（P＜0．01）；海马CA3区的正向弯曲型突触数显著减少，平坦型突触数显著增多（P＜0．05）．     

NAME对大鼠学习记忆过程中突触可塑性改变的影响∶超微结 …

用一次性被动回避反应和Ｍｏｒｒｉｓ水迷宫两种学习记忆模型,对大鼠侧脑室注射ＮＯＳ抑制剂Ｎ＾ｗ－ｎｉｔｒｏ－Ｌ－ａｒｇｉｎｉｎｅ（ＮＡＭＥ）前后海马ＣＡＩ区和大脑皮质额叶中突触形态的超微结构变化作了比较,结果发现：①在两种模型都观察到,单纯行为训练或人以ＮＡＭＥ,未能看到突触面积、囊泡直径以及突触界面曲度等较粗大的结构指标的改变;②但对于一些细微的结构指标,如突触后致密带厚度、突触间隙宽度以及其他一     

N型和Q型钙离子通道在海马突触传递中的作用

Ｎ型和Ｑ型钙离子通道在海马突触传递中的作用Ｎ型钙通道和一种药理学特性独特的Ｑ型钙通道被鉴定为支持海马ＣＡ３区与ＣＡＩ区神经元间突触传递的主要钙通道类型，而Ｌ型和Ｐ型钙通道对上述突触传递几乎没有贡献。发现于小脑颗粒细胞的Ｑ型钙通道据认为是由。；。一亚基...     

癫痫敏感大鼠脑内GFAP——免疫反应活性的变化

用红藻氨酸（ＫＡ）１０ｍｇ／ｋｇ（ｓ．ｃ）诱发大鼠出现癫病发作一个月后，经免疫细胞化学方法观察大鼠脑内神经胶质原纤维酸性蛋自（ＧＦＡＰ）－免疫反应产物的查化。发现海马的ＣＡ１，ＣＡ２，海马下脚和腹侧海马的海马门都位以及梨状皮层，内嗅皮层，隔区，杏仁核，伏隔核和尾核尾部的ＧＦＡＰ免疫染色阳性明显增强，这一现象可能与动物癫痫发作及发作后，癫痫敏感脑区的神经元损伤有关。     

大鼠脑缺血再灌流后海马氨基酸水平变化与神经元损害的关系探讨

目的探讨脑缺血再灌流后海马氨基酸递质变化与神经元损害的关系。方法建立大鼠前脑缺血再灌流模型,测定海马ＣＡ１区和ＣＡ３／齿状回区游离氨基酸含量,观察阻断隔－海马通路对海马神经元损害和氨基酸水平的影响。结果（１）海马结构中仅ＣＡ１区神经元明显损害,但ＣＡ１区和ＣＡ３／齿状回区的Ｇｌｕ、Ａｓｐ和ＧＡＢＡ含量无差异。（２）阻断隔－海马通路可明显减轻海马神经元损害,但对海马氨基酸水平变化无影响。结论脑缺血再灌流后,氨基酸递质水平的异常变化不是海马ＣＡ１区神经元选择性易损的唯一决定因素,隔－海马通路末梢释放的神经递质也参与海马神经元损害过程。     

癫痫患者智商和P300测试分析

目的探讨癫痫患者智商与Ｐ３００（Ｐ３）峰潜伏期（Ｐ３ＰＬ）之间的关系，并探讨怎样较合理地确定Ｐ３ＰＬ上限。方法对６６例２０～５０岁癫痫患者用修订韦氏智力量表（ＷＡＩＳ－ＲＣ）测出总智商（ＦＩＱ），按ＦＩＱ＜９０分（智能减低）和≥９０分（智能正常）将患者分为Ａ和Ｂ两个亚组；以纯音“ｏｄｄｂａｌ”刺激序列从Ｃｚ引出Ｐ３，测其峰潜伏期（ＰＬ）和波幅（Ａｍｐ）。以５０名年龄、性别、文化水平相匹配的志愿健康受试者为对照。结果（１）Ａ、Ｂ组与对照组，Ｐ３参量（ＰＬ、Ａｍｐ）差异均有显著意义（Ｐ＜０．０５，Ｐ＜０．０１），Ｐ３ＰＬ延长和Ａｍｐ降低均为Ａ组＞Ｂ组＞对照组；（２）Ｐ３ＰＬ用（ｘ＋２．０ｓ、ｘ＋２．５ｓ及ｘ＋３．０ｓ）三种不同上限时，在对智商的反映上有不同的敏感性和特异性。结论Ｐ３ＰＬ与智商有密切关系，但二者又不完全等同；在临床研究和筛选时，可能以ｘ＋２ｓ、ｘ＋２．５ｓ作上限为好；而用于临床实践时，以ｘ＋３ｓ为上限较佳     

尼莫地平对癫痫大鼠学习记忆及海马超微结构的影响

目的探讨尼莫地平(nimodipin,NIM)对戊四氮(pentylenetetrazol,PTZ)点燃癫痫大鼠学习记忆能力及海马CA3区超微结构的影响。方法动物分为正常对照组、PTZ组和NIM PTZ组,采用PTZ慢性点燃癫痫模型,应用Morris水迷宫观察各组大鼠空间学习记忆能力,电镜观察海马CA3区突触界面结构,并对突触活性参数量化分析。结果PTZ点燃癫痫大鼠存在学习记忆能力下降,其海马CA3区突触后致密物显著变薄、突触小泡显著减少、突触间隙显著增宽(P<0.05);尼莫地平能改善癫痫大鼠学习记忆障碍,与PTZ组比较,突触后致密物增厚、突触小泡增多、突触间隙变窄(P<0.05)。结论PTZ点燃癫痫大鼠存在空间学习记忆受损,可能与突触界面参数改变有关;NIM可以改善癫痫大鼠突触超微结构,提高学习记忆能力。     

Impaired maze performance in aged rats is accompanied by increased density of NMDA, 5-HT1A, and alpha-adrenoceptor binding in hippocampus

Using quantitative receptor autoradiography, we assessed binding site densities and distribution patterns of glutamate, GABA(A), acetylcholine (ACh), and monoamine receptors in the hippocampus of 32-month-old Fischer 344/Brown Norway rats. Prior to autoradiography, the rats were divided into two groups according to their retention performance in a water maze reference memory task, which was assessed 1 week after 8 days of daily maze training. The animals of the inferior group showed less long-term retention of the hidden-platform task but did not differ from superior rats in their navigation performance during place training and cued trials. The decreased retention performance in the group of inferior learners was primarily accompanied by increased alpha(1)-adrenoceptors in all hippocampal subregions under inspection (CA1-CA4 and dentate gyrus), while elevated alpha(2)-adrenoceptor binding was observed in the CA1 region and DG. Furthermore, inferior learners had higher NMDA binding in the CA2 and CA4 and increased 5-HT(1A) binding sites in the CA2, CA3, and CA4 region. No significant differences between inferior and superior learners were evident with regard to AMPA, kainate, GABA(A), muscarinergic M(1), dopamine D(1), and 5-HT(2) binding densities in any hippocampal region analyzed. These results show that increased NMDA, 5-HT(1A), and alpha-adrenoceptor binding in the hippocampus is associated with a decline in spatial memory. The increased receptor binding observed in the group of old rats with inferior maze performance might be the result of neural adaptation triggered by age-related changes in synaptic connectivity and/or synaptic activity.     

颞叶癫痫大鼠海马CA1区突触可塑性与空间记忆能力关系的研究

目的探讨颞叶癫痫大鼠海马CA1区突触超微结构与空间记忆能力改变的关系。方法以海人酸杏仁核微量注射建立经典的雄性Wistar大鼠颞叶癫痫化学点燃模型,分别于点燃后11d、17d、21d测定大鼠的空间记忆能力,并观察第21d海马CA1区神经毡突触超微结构变化。结果颞叶癫痫大鼠空间记忆能力减低,同时伴有海马CA1区神经毡内突触数密度降低(P<0．05),突触活性区膜面积缩小(P<0．05),突触界面曲率降低(P< 0．05),比表面减小(P<0．05),突触小泡数密度降低(P<0．05)。结论颞叶癫痫大鼠海马CA1区神经毡内突触损害和活力可能是导致其空间记忆能力下降的重要机制。     

吗啡戒断性焦虑大鼠海马突触界面结构及突触素表达变化

目的 探讨吗啡依赖戒断焦虑行为与海马CA1、CA3区突触界面结构和突触素表达变化之间的相关性.方法 剂量递增法建立大鼠吗啡依赖模型,高架十字迷宫检测焦虑行为,透射电镜技术结合图像分析系统、免疫组织化学比较对照组、模型组和治疗组(各6只)大鼠海马CA1、CA3区突触界面结构和突触素(P38)的表达.结果 (1)行为学:模型组开放臂的次数和时间均少于对照组和治疗组[最小有意义差异t检验(下同),P＜0.01或P＜0.05).(2)突触界面结构:模型组CA1区突触后致密物厚度[(10.7±0.9)nm]、突触活性区长度[(45±4)am]、突触间隙宽度[(3.80±0.30)nm]和突触界面曲率(1.37±0.12)均高于对照组和治疗组(P＜0.01或P＜0.05);模型组CA3区突触后致密物厚度[(12.7±1.1)nm]、突触活性区长度[(53±8)nm]、突触间隙宽度[(3.81 ±0.59)nm]、突触界面曲率(1.39±0.30)亦均高于对照组和治疗组(P＜0.01或P＜0.05).(3)突触素表达:模型组CA1、CA3区突触素吸光度(A)值分别为(0.42±0.06)和(0.43±0.05),显著高于对照组(0.2±0.02,0.25±0.03)和治疗组(0.27±0.04,0.26±0.03).结论吗啡戒断焦虑行为与海马CA1、CA3区突触形态结构可塑性及突触素表达水平有一定的相关性.     

Effects of movement training on synaptic interface structure in the sensorimotor cortex and hippocampal CA3 area of the ischemic hemisphere in cerebral infarction rats

BACKGROUND:Movement is an effective way to provide sensory,movement and reflectivity afferent stimulation to the central nervous system. Movement plays an important role in functional recombination and compensation in the brain. OBJECTIVE: To observe movement training effects on texture parameters of synaptic interfaces in the sensorimotor cortex and hippocampal CA3 area of the ischemic hemisphere and on motor function in cerebral infarction rats. DESIGN,TIME AND SETTING: This neural morphology and patholog...     

Effects of movement training on synaptic interface structure in the sensorimotor cortex and hippocampal CA3 area of the ischemic hemisphere in cerebral infarction rats★

BACKGROUND： Movement is an effective way to provide sensory, movement and reflectivity afferent stimulation to the central nervous system. Movement plays an important role in functional recombination and compensation in the brain. OBJECTIVE： To observe movement training effects on texture parameters of synaptic interfaces in the sensorimotor cortex and hippocampal CA3 area of the ischemic hemisphere and on motor function in cerebral infarction rats. DESIGN, TIME AND SETTING： This neural morphology and pathology randomized controlled animal experiment was performed at the Center Laboratory, Affiliated Hospital of Luzhou Medical College, China from November 2004 to April 2005. MATERIALS： A total of 32 healthy male Wistar rats aged 8 weeks were equally and randomly assigned into model and movement training groups. METHODS： Rat models of right middle cerebral artery occlusion were established using the suture occlusion method in both groups. Rats in the movement training group underwent balance training, screen training, and rotating rod training starting on day 5 after surgery, for 40 minutes every day, 6 days per week, for 4 weeks. MAIN OUTCOME MEASURES： Texture parameters of synaptic interfaces were determined using a transmission electron microscope and image analyzer during week 5 following model induction. The following parameters were measured： synaptic cleft width; postsynaptic density thickness; synaptic interface curvature; and active zone length. Motor function was assessed using balance training, screen training, and rotating rod training. The lower score indicated a better motor function. RESULTS： The postsynaptic density thickness, synaptic interface curvature, and active zone length were significantly increased in the sensorimotor cortex and hippocampal CA3 area of the ischemic hemisphere of rats from the movement training group compared with the model group （P 〈 0.05 or 0.01）. Curved synapses and perforated synapses were seen in the sensorimotor cortex and hippocampal CA3 area at     

Changes of synaptic ultrastructure in the guinea pig interpositus nuclei associate with response magnitude and timing after trace eyeblink conditioning

Learning-induced changes of synaptic ultrastructure have long been proposed as a mechanism that may contribute to support memory formation. Although recent studies have demonstrated that the interpositus nuclei (IN) play critical role in acquisition and retention of trace conditioned eyeblink responses (CRs), there is now limited evidence associating trace eyeblink conditioning with changes of synaptic ultrastructure in the IN. Here, we investigated this issue using a transmission electron microscope. Adult guinea pigs were randomly allocated to either a trace-paired, delay-paired, unpaired or exposure-only condition. The IN tissue was taken for morphological analysis 1 h after the completion of the tenth training session. Serial section analysis of synaptic ultrastructure revealed that trace eyeblink conditioning induced increases in the thickness of excitatory PSD. Classification of the synapses into shape subtypes indicated that the increased thickness of excitatory PSD was mainly attributable to increase in the concave- and convex-shaped synapses. On the contrary, trace eyeblink conditioning resulted in decreases in the thickness of inhibitory PSD. Specifically, these significant changes of PSD thickness were limited to occur in the animals with good behavioral performance. Further analysis of correlations between the trace CR performance and synaptic ultrastructural modifications showed that the thickness of excitatory PSD within the IN correlated with the peak amplitude of trace CRs, whereas the thickness of inhibitory PSD correlated with the onset latency. The present findings suggest that trace eyeblink conditioning induces structural plasticity in the IN, which may play a crucial role in acquiring and executing adaptive eyeblink movements.     

视皮层LTP诱导过程中的突触形态计量学研究

使用生后18～20天龄的幼年大鼠视皮层脑片标本，在LTP出现后半小时进行超微结构观察。运用白象分析仪分别对以下参数进行测量：（1）突触间隙的宽度；（2）突触后致密物（PSD）的厚度；（3）活性区的长度；（4）突触界面曲率。用双官法对突触数目进行计量，并用立体计量学方法对各种突触类型进行定量，结果显示：（1）LTP形成后半小时之内，突触反应增强，最大可达基础反应的516％；（2）PSD的厚度明显增厚；（3）活性区的面密度及突触界面曲率在备组间无明显差异；（4）穿孔性突触的数密度与对照组相比无显著差异；（5）总突触数目和棘突触数目的数密度较对照组明显增高。结果提示，PSD的增厚可能是LTI，诱导过程的形态学特征。在LTP的诱导过程中，突触数目有明显增加的趋势。