氯化锰抑制化学致痫剂诱发大鼠大脑皮层和海马神经元痫样放电

应用化学致痫剂马桑内酯诱发大鼠大脑皮质痫样放电,于侧脑室注射无要钙通道阻滞剂氯化锰后观察对致痫动物皮层脑电图、海马电图和皮层诱发电位的影响。结果表明,侧有离室注射无机钙通道阻滞剂氯化锰,可抑制致病大鼠皮层诱发电位的振幅和脑电图、海马电图痫样波的频率和振幅。提示氯化锰的作用可能与阻抑马桑内酯致痫时Ca^2 内流有关。     

电刺激蓝斑对马桑内酯诱发大鼠大脑皮层痫样放电的影响

采用皮层应用马桑内酯的方法致痫大鼠 ,观察电刺激蓝斑对皮层脑电图痫样波频率、振幅和大脑皮层诱发电位的影响。结果表明 ,电刺激蓝斑明显抑制马桑内酯诱发的痫样放电活动 ,侧脑室注射α受体阻断药酚妥拉明可明显抑制电刺激蓝斑的效应 ,注射 β受体阻断药心得安对电刺激蓝斑的效应影响不明显     

电刺激蓝斑对马桑内酯诱发大鼠大脑皮层痫？…

采用皮民桑内酯的方法致痫大鼠，观察电刺激蓝斑对皮层脑电图痫样波频率、振幅和大脑皮层诱发电位的影响。结果表明，电刺激蓝斑明显抑制马桑内酯诱发的痫样放电活动，侧脑室注射α受体阻断药酚妥拉明可明显抑制电刺激蓝斑的效应，注射β受体阻断药心得安对电刺激蓝斑的效应影响不明显。     

马桑内酯致痫大鼠海马IL-2免疫反应性的变化

目的:探求细胞因子中的白细胞介素2(Interleukin-2,IL-2)与癫痫发病之间的关系。方法:将Wistar大鼠分成三组,第一组侧脑室注入马桑内酯(Coriari Lactone,CL)2μL,第二组注入等量的生理盐水,第三组不做任何处理。然后运用免疫组织化学方法,对大鼠海马IL-2的免疫反应性进行分析;同时对实验中大鼠的行为及脑电图(eletroencepalograph,EEG)进行观察和记录。结果:第一组大鼠侧脑室注射CL过程中即诱发癫痫,且测到痫性脑电图,第二组、第三组无癫痫症状且未记录到痫性脑电图;第一组大鼠海马IL-2免疫反应性较第二组及第三组显著增强(P<0.01),表现在其海马CA_1、CA_2、CA_3区细胞数目增多,突起及其分支增多,着色明显加深;而第二、三组之间无明显差别(P>0.05)。结论:IL-2参与癫痫的发病过程,二者之间存在着一定的联系。     

安定在颞叶癫痫病灶的脑电图定侧定位中的应用

目的：总结安定在63例颞叶癫痫病灶的脑电图(elctroencephalogram EEG)定侧定位中的应用。方法：通过癫痫导联检查，明确63例患EEG表现双侧同步痫样放电，再进行美解眠诱发试验，当EEG显示示双侧同步痫样放电或临床发作时，停止注射美解眠，缓慢推注安定，持续描记EEG。结果：当安定注射到一定剂量，双侧同步痫样放电频率逐渐减少，能量降低，直至消失，但病灶侧侵于镜灶侧。当停止注射安定后，痫放电逐渐恢复，但病灶侧先于镜灶侧。结论：利用安定对痫灶放电的扩散产生抑制，但不能消除痫灶异常放电的作用原理，可以安全有效地对颞叶癫痫病灶进行定侧定位。     

睡眠中抽搐患者常规脑电图和动态脑电图比较

目的:比较睡眠中抽搐(含睡眠+清醒抽搐)患者常规脑电图(REEG)和24 h动态脑电图(AEEG)检出痫样放电及痫性放电率,从而指导临床医生选择脑电图检查方法。方法:常规脑电图组(I组)268例,描记清醒期30 min,动态脑电图组(II组)103例(其中75例由I组检查阴性转至),描记包括清醒期和睡眠期在内的24 h脑电图,统计两组的痫样放电率及痫性放电率并进行比较。结果:I组痫样放电56例(20.90%),II组痫样放电73例(70.87%);I组痫性放电3例(1.12%),Ⅱ组痫性放电13例(12.62%)。结论:动态脑电图组痫样放电及痫性放电率明显高于常规脑电图组(P<0.01),睡眠中抽搐(含睡眠+清醒抽搐)患者行24 h动态脑电图检查明显优于常规脑电图检查。     

强直电刺激海马致痫后大鼠大脑皮质NOS神经元变化研究

采用强直电刺激大鼠海马建立致痫模型,观察NOS神经元在致痫大鼠和正常大鼠大脑皮质的分布特征,探讨NO在癫痫发作中的作用。实验结果表明,建模组大脑皮质的阳性细胞数较正常组明显增多NOS神经元弥散分布于致痫大鼠大脑皮质,细胞胞体较大,并借突起相互交织成网。由此可得到如下结论：癫痫发生时脑内NO作用明显,这可能与癫痫引起的神经元损伤及NO介导的痫性放电的发生、传播、汇集有关;NOS—NO途径可能参与癫痫的启动与传播。     

胰岛素样生长因子-对大鼠脑缺血再灌注损伤后NSE含量变化影响

为了观察胰岛素样生长因子-(IGF-)对大鼠局灶性脑缺血再灌注不同时期海马皮层神经元特异性烯醇化酶(NSE)含量变化的影响,应用线栓法建立大鼠局灶性脑缺血再灌注损伤模型,将44只健康Spregue-Dawley(SD)大鼠随机分为假手术组(n=4)、缺血再灌注组和IGF-组。缺血再灌注组于脑缺血2h后根据再灌注不同时间(12h、24h、48h、72h、96h)分为5个亚组(每亚组4只);IGF-组于脑缺血2h侧脑室内注射IGF-10μg后也根据再灌注不同时间(12h、24h、48h、72h、96h)分为5个亚组(每亚组4只)。于各时间点处死大鼠,并采用酶联免疫分析法测定每只鼠缺血侧海马皮层NSE含量。结果显示,缺血再灌注12h和24h组缺血侧海马皮层NSE含量较假手术组明显下降(P<0.01),48h和72h组也有明显下降,但(P<0.05),96h组基本恢复到假手术组水平;脑缺血2h侧脑室内注射IGF-10μg后再灌注,48h和72h组与相应时间点缺血再灌注组比较明显上升(P<0.05),96h组基本恢复到假手术组水平。IGF-组NSE含量恢复比同时间点缺血再灌注组快,IGF-可能具有减轻缺血性脑损伤的作用。     

胰岛素样生长因子-Ⅱ对大鼠脑缺血再灌注损伤后NSE含量变化影响

为了观察胰岛素样生长因子-Ⅱ(IGF-Ⅱ)对大鼠局灶性脑缺血再灌注不同时期海马皮层神经元特异性烯醇化酶(NSE)含量变化的影响,应用线栓法建立大鼠局灶性脑缺血再灌注损伤模型,将44只健康Spregue-Dawley(SD)大鼠随机分为假手术组(n=4)、缺血再灌注组和IGF-Ⅱ组.缺血再灌注组于脑缺血2h后根据再灌注不同时间(12h、24h、48h、72h、96h)分为5个亚组(每亚组4只);IGF-Ⅱ组于脑缺血2h侧脑室内注射IGF-Ⅱ 10 μg后也根据再灌注不同时间(12h、24h、48h、72h、96h)分为5个亚组(每亚组4只).于各时间点处死大鼠,并采用酶联免疫分析法测定每只鼠缺血侧海马皮层NSE含量.结果显示,缺血再灌注12h和24h 组缺血侧海马皮层NSE 含量较假手术组明显下降(P＜0.01),48h 和72h组也有明显下降,但(P＜0.05),96h组基本恢复到假手术组水平;脑缺血2h侧脑室内注射IGF-Ⅱ 10μg后再灌注,48h 和72h组与相应时间点缺血再灌注组比较明显上升(P＜0.05),96h组基本恢复到假手术组水平.IGF-Ⅱ组NSE含量恢复比同时间点缺血再灌注组快,IGF-Ⅱ可能具有减轻缺血性脑损伤的作用.     

家兔杏仁基底核V1区神经电活动的研究

在１０只乌拉坦麻醉和三碘季胺酚麻痹的新西兰兔上用粗金属电极记录刺激杏仁在视皮层Ｖ１区的诱发电位活动，并考察其分布情况。当刺激杏仁基底核时，在整个视皮层Ｖ１区都记录到潜伏期为１￣２ｍｓ的诱发电位，振幅最大的电位分布在Ｖ１区前部。刺激杏仁基底核还使视皮层光诱发电位的主反应受到抑制，作用的潜伏期为１０ｍｓ，时程为２０ｍｓ。这此结果显示，杏仁基底核可能有向视皮层Ｖ１区直接的纤维联系，其功能之一可能是介导杏     

Optical imaging of epileptiform and functional activity in human cerebral cortex.

Optical imaging of animal somatosensory, olfactory and visual cortices has revealed maps of functional activity. In non-human primates, high-resolution maps of the visual cortex have been obtained using only an intrinsic reflection signal. Although the time course of the signal is slower than membrane potential changes, the maximum optical changes correspond to the maximal neuronal activity. The intrinsic optical signal may represent the flow of ionic currents, oxygen delivery, changes in blood volume, potassium accumulation or glial swelling. Here we use similar techniques to obtain maps from human cortex during stimulation-evoked epileptiform afterdischarges and cognitively evoked functional activity. Optical changes increased in magnitude as the intensity and duration of the afterdischarges increased. In areas surrounding the afterdischarge activity, optical changes were in the opposite direction and possibly represent an inhibitory surround. Large optical changes were found in the sensory cortex during tongue movement and in Broca's and Wernicke's language areas during naming exercises. The adaptation of high-resolution optical imaging for use on human cortex provides a new technique for investigation of the organization of the sensory and motor cortices, language, and other cognitive processes.     

初孵扬子鳄大脑皮层组织学结构观察

本文用光镜对扬子鳄大脑皮层的组织学结构进行了研究 .扬子鳄大脑皮层可分为外网状层、细胞层和内网状层三层 ,神经细胞绝大多数集中于细胞层内 ,内、外网状层中零星分布一些小细胞 .从内侧到外侧 ,大脑皮层可分为海马、新皮质和梨状皮质三部分 ,三者之间无明显界线 ,细胞排布有所区别 .本文对扬子鳄的大脑皮层同其他脊椎动物的进行了比较讨论 .     

89次额叶癫痫发作期Video-EEG监测报告

利用ZN80 0 0型Video EEG监测系统对 10例额叶癫痫患者进行脑电和行为监测 ,旨在探讨额叶癫痫发作时的行为表现及脑电变化特征。结果表明 :额叶癫痫发作以运动症状为主 ,常于夜间发作 ,发作频繁而短暂。发作期EEG为额区癫痫样放电亦可为高幅慢波 ,与临床发作同步     

基于重复经颅磁刺激的脑功能网络分析

基于脑功能网络探究重复经颅磁刺激对大脑皮层神经交互作用的影响.利用基于图论的复杂网络理论,进行了经颅磁刺激作用于皮层所诱发脑电信号的脑功能网络分析.采用重复刺激对大脑运动区进行刺激,分别构建了安静状态下、磁刺激运动区状态下的脑电信号的脑功能网络,对脑功能网络全局参数和局部参数进行了图像直观表述和统计学分析.结果发现,磁刺激运动区状态下相比于安静状态下的脑功能网络全局参数和局部参数都发生了明显改变,经统计学分析对比具有显著性差异.     

电刺激大鼠mPFC对听皮层神经元听反应的影响

实验在40只成年SD大鼠上进行,使用常规电生理学方法,观察了电刺激大鼠内侧额叶前皮质(medial prefrontal cortex, mPFC)对听皮层神经元听反应的影响.在122个神经元上观察了电刺激mPFC对听反应的影响.对其中93个神经元作了详细分析发现,有73个神经元的听反应受到易化（39个,41.9%）或抑制（34个,36.6%）.刺激mPFC对听反应的影响存在最佳刺激间隔,大多数神经元（51个,69%）在10~15 ms之间.结果提示,大鼠mPFC可对听皮层神经元的听反应调制,这种调制可能是通过多级神经元环路实现的.     

Cholinergic-rich brain transplants reverse alcohol-induced memory deficits

Alcohol-induced memory impairment in man has been attributed to deficiencies in subcortical noradrenergic and cholinergic systems, as well as to damage in midbrain structures. Korsakoff's psychosis, a disease in which alcohol poisoning causes apparently irreversible memory defects, is characterized by lesions in cholinergic and noradrenergic nuclei and by a decrease in the activity of choline acetyltransferase (ChAT) and the content of noradrenaline (NA) in forebrain areas such as cerebral cortex and hippocampus, innervated by these nuclei. Prolonged intake of ethanol in rodents similarly produces signs of noradrenergic and cholinergic deafferentation in the cortex and hippocampus, as well as persistent memory deficits. To test whether alcohol-induced memory impairments depend on cholinergic deafferentation, we transplanted cholinergic-rich fetal basal forebrain cell suspensions into the cortex and hippocampus of alcohol-treated rats. The substantial and persistent memory losses produced in our rats by ethanol intake were associated with an impairment of cholinergic function, and were reversed by cholinergic-rich transplants into cortex and hippocampus.     

中缝背核对躯体反射放电的影响

作者在清醒麻痹的猫上进行中缝背核对躯体反射放电影响的实验。结果表明:电刺激猫中缝背核(DR)对躯体反射放电活动具有明显地抑制作用;对躯体伤害性刺激引起的丘脑束旁核(PF)诱发单位放电活动亦具有明显地抑制作用。     

Functional localization and lateralization of human olfactory cortex.

Anatomical and physiological investigations in monkeys indicate that olfaction is subserved by several cortical regions. But the areas implicated in the human olfactory system have not been definitively identified by functional criteria. Behavioural evidence has suggested that laterally specialized mechanisms for odour processing may exist, but the neuroanatomical substrate remains unknown. We used positron emission tomography to study the cortical representation of human olfactory processing by comparing cerebral blood flow changes evoked during olfactory stimulation with those of a control task. We report here significant cerebral blood flow increases at the junction of the inferior frontal and temporal lobes bilaterally, corresponding to the piriform cortex, and unilaterally, in the right orbitofrontal cortex. The results complement and extend previous data implicating these regions in olfactory processing, and indicate that a functional asymmetry exists in the human brain favouring the right orbitofrontal area in olfaction.     

An insulinoma with clinical and electroencephalographic features resembling complex partial seizures

We described a female patient with insulinoma who experienced recurrent episodes of automatism, confusion and convulsion. Furthermore, her electroencephalography （EEG） findings resembled the pattern in complex partial seizures with secondary generalization. The interictal EEG showed spikes and sharp waves, as well as focal slowing over the left temporal lobe, and the ictal EEG revealed generalized spikes and sharp waves associated with diffused slowing. She was initially misdiagnosed as pharmacoresistant epilepsy. After the insulinoma was found and surgically removed, her EEG turned normal and she was seizure-free during the 4-year follow-up. This report highlights the need for careful reassessment of all seizures refractory to medication, even for the oatients associated with eoileotiform discharges on EEG.