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find Keyword "海马" 47 results
  • Effect of Lidocaine-induced Seizure on Spatial Learning Memory in Rats

    目的 研究利多卡因对海马的神经毒性是否会对大鼠空间学习记忆能力产生影响,并探讨大鼠空间学习能力的变化与海马CA3区锥体细胞数目的相关性。 方法 将成年Wistar雄性大鼠随机分为基础值组(n=7)和利多卡因惊厥组(n=40)。基础值组大鼠静脉给予生理盐水后使用Y迷宫测定大鼠的空间学习能力。利多卡因惊厥组大鼠尾静脉持续输注利多卡因造成惊厥,待大鼠恢复正常运动以后放入鼠笼重新饲养。并于惊厥后第1、3、5、7天从中随机抓取大鼠测试其空间学习能力以及组织学改变。根据对应天数将利多卡因惊厥组的40只大鼠随机细分为Day-1、Day-3、Day-5、Day-7亚组,每亚组10只。所有大鼠在测定空间学习能力之后立即处死,取出大脑并做石蜡包埋,冠状面切片后进行组织学检测,显微镜下评估海马CA3区锥体细胞状态。 结果 ① 基础值组和Day-1、Day-3、Day-5、Day-7亚组大鼠的Y迷宫穿梭次数分别为(25.2 ± 3.7)、(27.1 ± 8.1)、(36.9 ± 9.9)、(38.7 ± 10.6)、(40.6 ± 16.3)次,除Day-1亚组与基础值组比较差异无统计学意义(P>0.05)外,其余各亚组与基础值组差异均有统计学意义(P<0.05);② 与基础值组单位面积(10.3 ± 4.5)个(异常锥体)细胞比较,利多卡因惊厥组大鼠海马CA3区异常锥体细胞数增加,Day-1、Day-3、Day-5、Day-7亚组计数值分别为13.0 ± 7.2、15.6 ± 5.0、19.6 ± 8.1、18.1 ± 5.1,且与大鼠Y迷宫穿梭次数呈正相关(r=0.711,P<0.05)。 结论 利多卡因引起的惊厥使成年大鼠海马依赖性空间学习能力下降,利多卡因的神经毒性引起的海马异常锥体细胞增多可能是造成这一现象的一种原因。

    Release date:2016-09-08 09:13 Export PDF Favorites Scan
  • 颞叶癫痫的海马网络功能连接

    由于海马和其他颞叶结构与其他脑区存在连接, 颞叶癫痫(TLE)可以影响到颞叶以外的结构。采用磁共振(MRI)功能连接的方法来探索TLE海马网络的变化, 以更全面的分析TLE的异常分布范围。共纳入三组被试:左侧颞叶癫痫TLE组(13例); 右侧TLE组(11例)及健康对照组(16例)。分别在这三组被试中划定左、右两侧海马为感兴趣区(Regions of interest, ROIs)。通过测定静息态功能磁共振(functional MRI, fMRI)低频血氧水平(Blood oxygenation level dependent, BOLD)信号的相关性来寻找与ROIs存在着功能连接的脑区。采用独立样本t检验进行组间对比。在TLE中, 海马与多个脑区功能连接增强, 包括边缘系统中的几个关键区域(颞叶、岛叶、丘脑)、额叶、角回、基底节、脑干和小脑, 同时海马与一些脑区之间的功能连接减弱, 包括感觉运动皮质(视觉、体感、听觉、初级运动)和默认网络(楔前叶)。左侧TLE的功能连接改变较右侧TLE更为明显。TLE功能连接改变揭示了TLE累及多个脑区, 导致大脑神经网络功能失常。左侧TLE和右侧TLE的海马功能连接存在显著差异。

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  • 海马硬化与癫痫

    难治性癫痫的患者常常伴有海马硬化, 是耐药性癫痫的主要致病因素。海马硬化在长期复杂的癫痫发作过程中逐渐形成, 两者之间的作用关系一直是癫痫领域的研究热点。现结合近年来国内外研究的新进展探讨海马硬化与癫痫之间的关系, 为颞叶癫痫的临床诊疗提供新的思路

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  • Neuroprotective effects and mechanisms of selective histone deacetylases inhibitor MS-275 on lithium-pilocarpine induced seizures in rats

    ObjectiveTo investigate the neuroprotective effects and mechanisms of selective histone deacetylases inhibitor MS-275 on rats after seizures. MethodsA total of 75 rats were randomly divided into 5 groups for treatment:control group,pilocarpine group, treatment group Ⅰ(administered with MS-275, 20mg/kg, once a day,intraperitoneally in 7 consecutive days), treatment group Ⅱ(administered with MS-275, 40mg/kg, once a day, intraperitoneally in 7 consecutive days), MS-275 pretreatment group. We used lithium and pilocarpin to induce seizures. Behaviors of rats in each group were observed. At 72 hours after seizures, Nissl staining and immunohistochemical were respectively used to evaluate the loss of neurons and histone acetylation levels of hippocampal CA1 and CA3 regions in each group. Escape latency in the control group, treatment group Ⅰ, treatment group Ⅱ and MS-275 pretreatment group were longer than pilocarpine group(P<0.05). ResultsCompared with the pilocarpine group, rats in MS-275 pretreatment group could delay pilocarpine-induced seizures and reduce mortality (P<0.05). Degree of neuronal loss and degeneration in both treatment group Ⅰ and treatment group Ⅱ were reduced compared with the pilocarpine group (P<0.05) and the level of histone acetylation in hippocampal CA1 and CA3 regions of the rats were increased compared with the pilocarpine group (P<0.05). ConclusionHDACs inhibitors MS-275 can improve the neuronal damage, histone deacetylation of rats' brain and rats cognitive decline, which can exert an neuroprotective effect on rats after seizures, whose mechanism may be related to its antiinflammatory effect.

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  • 海马苔藓纤维出芽分子机制及在颞叶癫痫中的作用

    颞叶癫痫是难治性癫痫中最常见的类型,苔藓纤维出芽(Mossy fiber sproutinggranular, MFS)是颞叶癫痫患者最特征性的病理变化,但其分子信号通路及在颞叶癫痫中的作用至今还未明确。现综述近年有关MFS的信号通路及其在颞叶癫痫中作用。首先从颗粒细胞轴突出芽相关的信号通路进行阐述,主要包括细胞外信号调节激酶通路调节神经元胞体和轴突生长发育的作用,还有雷帕霉素靶蛋白转导通路对痫性发作的影响以及调节细胞增殖、突触重塑的作用。然后进一步阐述MFS到底促进还是抑制癫痫的发生以及与颞叶癫痫的因果关系。为颞叶癫痫的发生机制及治疗提供新思路。

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  • 颞叶癫痫动物模型

    癫痫是一种神经系统常见疾病,绝大多数癫痫患者可以通过药物控制发作,但是仍有约1/3患者为药物难治性癫痫,在难治性癫痫中绝大多数为颞叶癫痫。对颞叶癫痫动物模型的研究有助于了解其发病机制、脑电改变及病理生理特点,为寻找其治疗方法有一定帮助。现就颞叶癫痫动物模型的制作方法、行为学表现、脑电改变及病理特征进行总结。目前常用颞叶癫痫动物模型有海人酸模型和匹罗卡品模型,两种模型均可以通过系统给药和局部给药方式实现,可以诱发急性癫痫持续状态,之后出现反复自发发作从而形成慢性癫痫模型。两种模型均可引发海马起源的痫样放电,造成海马神经元变性、胶质细胞增生及苔藓纤维出芽,与人类颞叶癫痫相似。

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  • Arc调控神经元突触可塑性作用

    癫痫是常见的神经系统疾病之一,为脑部神经元高度同步化异常放电,其发病机制尚不明确。海马结构的苔藓纤维出芽和突触重塑学说是其形成的主要病理基础,也是癫痫长期、反复发作的重要原因。活性调节的细胞骨架蛋白(Activity regulated cytoskeletal protein,Arc)是一种谷氨酸神经元突触后细胞骨架相关蛋白,属于即刻早期基因,在脊椎动物中高度保守,被认为是参与突触重塑的重要因子。现将Arc的表达转录特征、Arc参与神经元细胞突触可塑性的结构性和功能性改变、突触可塑性参与海马苔藓纤维出芽诱发癫痫的发病、Arc通过调控海马神经元细胞突触可塑性及MFS参与癫痫的发病进行阐述,为研究Arc的突触可塑性作用为阐明癫痫致病机制提供新的方向和思路。

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  • Roles of Hippocampal long-term potentiation in chronic cognitive dysfunction of immature epileptic rats

    ObjectiveTo investigate the effects of hippocampal long-term potentiation (LTP) on cognitive dysfunction in immature epileptic rats. MethodsImmature epileptic rats were established by intraperitoneal injection of lithium chloride-pilocarpine (li-pilo). Racine classification standard modified by Becker was used to evaluate behavior of epileptic seizure, and the survival rats within RacineⅣmagnitude were selected in the experiment. The function of learning and memory of epileptic rats when they were adult was assessed using Morris water maze experiment, and their independent exploratory behavior was evaluated by the open-field test. Field potential was recorded by electrophysiological technology to detecte whether hippocampal LTP was essential of cognitive dysfunction. ResultsThe function of learning and memory was significantly impaired when compared with controls(n=8, t=10.86, P < 0.05;n=8, t=9.98, P < 0.05). In addition, independent exploratory behavior was significantly reduced when compared with controls(n=8, t=12.89, P < 0.05). Besides, CA1 hippocampal LTP induced by high-frequency stimulation presented the significant inhibition in epileptic rats with cognitive dysfunction when compared with controls(Slope:n=8, t=13.32, P < 0.05;Amplitude:n=8, t=20.02, P < 0.05). ConclusionInhibition of CA1 hippocampal LTP may be implicated in cognitive dysfunction of epileptic rats.

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  • The dynamic expressional changes of neuronal growth and differentiation-associated miR-124a and miR-9 in the process of epileptogenesis

    ObjectiveTo explore the dynamic expression changes of neuronal growth and differentiation-associated miR-124a and miR-9 in the process of epileptogenesis. MethodsEstablish the lithium-pilocarpine induced status epilepticus (SE) rat model. Animal behavior change induced by SE as well as in the period of chronic epilepsy was observed by naked-eye or video-recording. Major time points for the study were chosen at 1d, 7d, 14d and 28d post-SE, on which the post-SE rats were decapitated and their hippocampal specimens were obtained. Total RNA from each specimen was extracted and qPCR was exploited to detect miR-124a and miR-9 expression in the specimens. Statistical analysis was used to show the dynamic expressional changes of miR-124a and miR-9 in rat hippocampus at 1d, 7d, 14d and 28d post-SE during the process of epileptogenesis. ResultsCompared with normal rats, the expression level of miR-124a in rat hippocampus did not show a significant difference at 1d post-SE, but it had shown markedly differences at 7d, 14d and 28d post-SE(P < 0.05), with a declining trend. Compared with normal rats, the expression level of miR-9 had demonstrated significant differences at 1d, 7d, 14d and 28d post-SE(P < 0.05)with a generally increasing trend, although there was slight fluctuation of expressional up-regulation at 7d post-SE. ConclusionNeuronal growth and differentiation-associated miR-124a and miR-9 had shown dynamic changes of down-regulation or up-regulation in the process of epileptogenesis. It can be suspected that miR-124a and miR-9 take part in hippocampal neurogenesis post-SE and be involved in epileptogenesis process.

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  • Risks of seizure recurrence from antiepileptic drug withdrawal among seizure-free patients for more than three years

    ObjectiveTo determine the outcome of antiepileptic drugs (AEDs) withdrawal in patients who had been seizure-free for more than two years. MethodsPatients with epilepsy who had been seizure-free for at least two years and decided to stop AEDs therapy gradually were checked on every two months for seizure relapse. The inclusion criteria were:①diagnosis of epilepsy, defined as at least two unprovoked seizures at least 24 hours apart; ②patients remained seizure-free for at least 24 consecutive months during AEDs therapy; ③patients expressed a desire to discontinue AEDs therapy gradually and agreed to return for regular follow-ups; and④electroencephalogram (EEG) showed no epileptic discharge. The time to a seizure relapse and predictive factors were analyzed by survival methods, including sex; age at seizure onset; number of episodes; seizure-free period before AEDs withdrawal; duration of follow-up after AEDs withdrawal; AEDs tapering off period (taper period); results from brain MRI; EEG before seizure-free; EEG before drug withdrawal; seizure type (classified as generalized, partial, or multiple types based on history); the number of AEDs administered for long-term seizure control. A log-rank test was used for univariate analysis, and a Cox proportional hazard model was used for multivariate analysis. ResultsSixty-eight patients (39 male, 29 female) were admithed. The relapsed rate was 23.5%. Univariate analysis and multivariate Cox regression analysis indicated that multiple AEDs, hippocampal sclerosis and withdrawal time were significantly correlated with seizure recurrence and those were significant independent predictive factors, with hazard ratio were 0.861, 2.223 and 2.137 respectively. ConclusionsThe relapsed rate in our study was similar to other studies. Distinguishing variables, such as multiple AEDs, hippocampal sclerosis and withdrawal time, need to be considered when decide to withdraw. Therefore, our recommendation is that after two years of being seizure-free, patients could consider withdrawal unless they are hippocampal sclerosis patients.

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