胞二磷胆碱、氯脂醒、神经节苷脂(GM1)对青霉素致痫大鼠脑内某些内源性物质的影响

目的 探讨胞二磷胆碱、氯脂醒、神经节苷脂（GM1）对青霉素致痫大鼠脑内某些内源性物质的影响，为其临床应用提供依据。方法 将35只成年健康SD大鼠随机分为5组：对照组、模型组、胞二磷胆碱组、氯脂醒组、GM1组。制作癫痫模型，制模后1h处死大鼠，取额顶叶脑皮质测定其中超氧化物岐化酶（SOD）、丙二醛（MDA）、谷氨酸（Glu）、γ-氨基丁酸（GABA）含量。结果 ①模型大鼠均制模成功，腹腔注射胞二磷胆碱（500mg／kg）、氯脂醒（100mg／kg）、GM1（30mg／kg）预处理均不能阻止青霉素诱导的大鼠癫痫发作。②与对照组相比，模型组大鼠脑皮质内SOD活性明显降低，MDA、Glu、Glu／GABA值含量明显升高（P〈O．05或尸〈0．01）。③与模型组相比，胞二磷胆碱组、氯脂醒组、GM1组大鼠脑皮质内SOD活性明显升高，MDA、Glu／GABA值含量明显降低（P〈0．05），GM1组Glu含量亦明显降低（P〈0．05）。结论 胞二磷胆碱、氯脂醒、GM1虽不能预防青霉素诱导的大鼠癫痫发作，但可提高其脑组织清除自由基、增强抗氧化以及调节神经递质紊乱、减轻兴奋性氨基酸的毒性等作用，从而起到保护作用。     

激光氧液对癫痫持续状态大鼠海马组织MDA、SOD动态变化的影响及疗程选择

目的观察激光氧液对戊四氮（PTZ）所致癫痢持续状态（SE）大鼠海马组织丙二醛（MDA）和超氧化物歧化酶（SOD）的影响及激光氧液的疗程选择。方法28日龄雄性SD大鼠以PTz建立癫痫持续状态模型,随机分为PTz＋激光氧液组、PTz＋GS组和NS＋激光氧液组、NS＋GS组,分别给予激光氧液和5％葡萄糖液（5％GS）尾静脉输入,于模型制作成功后第0、3、7、10、14天采用比色法检测MDA含量和SOD活力。结果（1）MDA结果：PTZ＋GS组大鼠海马组织MDA含量在SE后3d、7d、10d、14d较Ns＋GS组明显增高（P〈0．05）,PTz＋激光氧液组与之趋势相同,但在各时间点均较PTZ＋GS组大鼠降低（P〈O．05）。（2）SOD结果：PTZ＋GS组大鼠海马组织SOD活力在SE后3d、7d较NS＋GS组明显降低（P〈0．05）,PTZ＋激光氧液组s0D活力与之趋势相同,但在3d、7d、10d三个时间点上较PTZ＋GS组大鼠升高（P％0．05）。第14天各组大鼠海马内SOD活力均无统计学差异（P〉0．05）。结论（1）激光氧液能降低SE大鼠MDA含量,升高SOD活力。（2）激光氧液的治疗可选择10d为一疗程。     

戊四氮致癫痫状态对大鼠长期行为和脑电的影响

目的 建立一种戊四氮（ＰＴＺ）致癫痫状态（ＳＥ）模型,并探讨ＰＴＺ致惊厥与癫痫形成之间的关系。方法 观察ＰＩＺ致抽搐发作（抽搐组）和ＰＴＺ致抽搐延长发作即癫痫状态（ＳＥ组）对大鼠长期行为和脑电（ＥＥＧ）的影响,同时观察二者是否产生海马、皮质神经元损伤。结果 ＰＴＺ致抽搐延长发作能够产生具有某些癫痫特征的长期效应,如自发痫样放电、惊厥阈下剂量ＰＴＺ可诱导癫痫发作以及皮质和海马神经元损伤,而单次抽搐发     

锂-匹罗卡品致癫大鼠早期大脑皮质MyT1 mRNA表达变化

目的 探讨氟化锂-匹罗卡品致癫大鼠脑髓鞘转录因子1基因表达变化及其意义。方法 以氯化锂、匹罗卡品对雄性成年SD大鼠先后腹腔注射，制成癫痫持续状态动物模型；采用5′末端标记地高辛的寡核苷酸探针荧光原位核酸分子杂交检测癫性发作后早期大鼠大脑皮质MyT1 mRNA阳性细胞数量。结果 与对照组相比，癫痫后1d组大鼠脑皮质MyT1 mRNA阳性细胞数减少（P＜0.05）；其他各组大鼠脑皮质MyT1 mRNA阳性细胞数都有明显的增加，其中癫痫后7d和14d组MyT1mRNA阳性细胞数都有非常显著的增加（P＜0.05，P＜0.01）。结论 氯化锂-匹罗卡品致癫大鼠早期大脑MyT1 mRNA表达增加，并有时程性变化，提示与早期脑损伤修复有关。     

一氧化氮和一氧化氮合酶在鼠脑内形成吗啡依赖的作用研究

目的：研究一氧化氮（NO）和一氧化氮合酶（NOS）在吗啡依赖形成中的作用。方法;对吗啡依赖和戒断大鼠脑内NO含量和NOS活力进行测定。结果：未发现吗啡依赖和戒断大鼠脑内NO含量和NOS活力有改变。结论：对NO／NOS与吗啡依赖的关系还有待进一步研究。     

川芎嗪对脑挫伤大鼠脑组织MDA、SOD、NO及含水量影响的研究

目的 观察川芎嗪对脑挫伤大鼠脑组织中丙二醛（MDA）、超氧化物歧化酶（SOD）、一氧化氮（NO）含量及脑组织含水量的影响，探讨川芎嗪在治疗脑挫伤中的应用。方法 建立自由落体大鼠脑挫伤模型，治疗组脑挫伤后第2天开始应用川芎嗪腹腔注射治疗，对照组腹腔注射等量生理盐水．连续应用6d。正常组不致伤。检测治疗组、对照组及正常组大鼠脑组织中MDA、SOD、NO含量及脑组织含水量，并进行统计分析。结果 脑挫伤后大鼠脑组织中MDA、NO含量及脑组织含水量较正常组增高，SOD含量较正常组降低（P〈0．05）。川芎嗪治疗组大鼠脑组织中MDA、NO含量及脑组织含水量较对照组显著降低，SOD含量较对照组显著上升（P〈0．05）。结论 川芎嗪能够有效提高挫伤后脑组织中SOD含量，减少MDA及NO含量产生．有效改善脑水肿，从而发挥治疗作用。     

依达拉奉对癫痫大鼠脑内谷氨酸的影响

目的 探讨依达拉奉对戊四氮致痫大鼠脑中谷氨酸的影响.方法 30只成年SD大鼠随机分为对照组、癫痫组和治疗组,癫痫组和治疗组大鼠腹腔注射戊四氮60mg/kg,诱导癫痫发作.治疗组于注射戊四氮之前1h经腹腔注射依达拉奉30mg,并观察1h.然后处死大鼠取脑,应用柱前衍生HPLC-荧光法测定大鼠脑皮质谷氨酸(Glu)的含量.结果 治疗组痫性发作潜伏期、平均痫性发作等级及脑内谷氨酸含量与癫痫组相比差异均有显著性(P<0.01).结论 依达拉奉可以通过拮抗氧自由基并抑制谷氨酸的释放,在癫痫发作中发挥保护作用.     

脑囊尾蚴病患者脑脊液特异性IgG、一氧化氮含量与高颅压和癫(癎)的关系

目的探讨脑囊尾蚴病患者脑脊液（CSF）特异性IgG含量和一氧化氮（NO）水平与高颅压和癫痫的关系。方法检测40例脑囊尾蚴病患者CSF特异性IgG的含量和NO的水平,并对有无高颅内压征及癫痫的患者进行比较、分析。另外,检测23例大隐静脉曲张患者（对照组）CSFNO水平作对照。结果与对照组相比,脑囊尾蚴病组CSF中NO值明显增高（P〈0.01）。脑囊尾蚴病组特异性IgG与NO水平呈正相关（r=0.579,P〈0.05）;高颅内压患者CSF中特异性IgG与NO水平显著高于无高颅内压患者（P〈0.05-0.01）;癫痫患者CSF中NO值与无癫痫患者相比明显升高（P〈0.05）,而特异性IgG含量虽然升高但差异无统计学意义（P〉0.05）。结论脑囊尾蚴病致颅内高压征患者CSF中NO和特异性IgG水平明显增高;脑囊尾蚴病致癫痫患者CSFNO水平亦增高。     

己酮可可碱对癫痫大鼠黑质多巴胺能神经元的影响

目的观察己酮可可碱(Ptx)预处理对癫痫发作大鼠多巴胺(DA)能神经元的影响。方法健康、成年雄性Wistar大鼠分为3组:对照组、癫痫组和Ptx预处理组(PTX组)。对照组腹腔注射生理盐水(127mg·kg~(-1));癫痫组和PTX组大鼠用氯化锂-匹罗卡品(Li-Pc)诱发癫痫发作,先腹腔注射氯化锂(Li,127mg·kg~(-1)),20h后背部皮下注射匹罗卡品(Pc,20mg·kg~(-1));PTX组大鼠在Pc注射前30min通过腹腔给予Ptx(60mg·kg~(-1))。观察大鼠癫痫发作情况;利用免疫细胞化学、蛋白印迹和液质联用检测黑质(SN)DA能神经元功能活动;通过分光光度法检测SN和尾壳核(CPu)处丙二醛(MDA)、谷胱甘肽(GSH)含量及超氧化物岐化酶(SOD)活性,探讨Ptx预处理对Li-Pc诱发癫痫大鼠DA能神经元的影响及氧化应激的参与。结果 (1)Ptx预处理降低了Li-Pc诱发大鼠的癫痫发作率,显著延长了大鼠的癫痫发作潜伏期(P0.01);(2)免疫细胞化学和蛋白印迹显示癫痫组大鼠SN和CPu处TH免疫反应强度和蛋白含量比对照组明显降低;与癫痫组相比,PTX组大鼠SN和CPu的TH免疫反应强度和蛋白含量显著增加(均P0.05);(3)癫痫组大鼠CPu的DA、二羟苯乙酸(DOPAC)和高香草酸(HVA)含量较对照组明显降低;与癫痫组相比,PTX组大鼠DA、DOPAC和HVA含量显著增加(均P0.05);(4)与对照组相比,癫痫组大鼠SN和CPu的MDA含量明显增多,GSH含量明显减少,SOD活性显著降低;与癫痫组相比,PTX组大鼠SN和CPu的MDA含量明显降低,GSH含量和SOD活性明显升高(均P0.05)。结论 Ptx预处理缓解了Li-Pc诱发癫痫大鼠脑内的氧化应激状态和DA能神经元功能活动的降低。     

实验性癫痫大鼠不同脑区的L-ENK表达及意义

目的 采用戊四氮（PTZ）雳发大鼠癫痫。动态观察了部分脑区亮氨酸-脑啡肽（L-ENK）含量的变化，以探讨L-ENK与癫痫的关系。方法 清洁级近交系雄性SD大鼠50只，分为对照组（A组，10只）及实验组（40只）。实验组按体重50mg／kg腹腔注射PTZ1次，对照组腹腔注射同等容量的生理盐水。根据癫痫发作分级，0～1级7只为B组，立即取脑；2级以上发作33只，随机于癫痫发作后0h（C组，10只），6h（D组，11只），24h（E组，10只）取脑；最后剩下2只（F组）72h取脑。采用放射免疫方法，动态观察脑组织中海马、中脑、纹状体和额叶中L-ENK的改变；S-P免疫组化染色法染色，观察各组大鼠海马CAI区L-ENK的表达。结果 发现应用PTZ后，癫痫大发作大鼠及末出现大发作的大鼠额叶、海马、中脑及纹状体中L-ENK含量均明显升高，两组间除中脑外无明显差异；但大发作大鼠的海马、中脑及纹状体L-ENK含量显著高于对照组。大发作后各脑区的L-ENK含量呈逐渐下降的过程。结论 L-ENK可能参与了癫痫的发生过程。     

Dynamic fMRI and EEG recordings during spike-wave seizures and generalized tonic-clonic seizures in WAG/Rij rats.

Generalized epileptic seizures produce widespread physiological changes in the brain. Recent studies suggest that "generalized" seizures may not involve the whole brain homogeneously. For example, electrophysiological recordings in WAG/Rij rats, an established model of human absence seizures, have shown that spike-and-wave discharges are most intense in the perioral somatosensory cortex and thalamus, but spare the occipital cortex. Is this heterogeneous increased neuronal activity matched by changes in local cerebral blood flow sufficient to meet or exceed cerebral oxygen consumption? To investigate this, we performed blood oxygen level-dependent functional magnetic resonance imaging (fMRI) measurements at 7T with simultaneous electroencephalogram recordings. During spontaneous spike-wave seizures in WAG/Rij rats under fentanylhaloperidol anesthesia, we found increased fMRI signals in focal regions including the perioral somatosensory cortex, known to be intensely involved during seizures, whereas the occipital cortex was spared. For comparison, we also studied bicuculline-induced generalized tonic-clonic seizures under the same conditions, and found fMRI increases to be larger and more widespread than during spike-and-wave seizures. These findings suggest that even in regions with intense neuronal activity during epileptic seizures, oxygen delivery exceeds metabolic needs, enabling fMRI to be used for investigation of dynamic cortical and subcortical network involvement in this disorder.     

Activity of alpha and gamma extensor motor axons during metrazol-induced seizures in cat

Efferent discharges were recorded in nerves to extensor and flexor muscles simultaneously with EEG of contralateral motor area during Metrazol-induced seizures in anesthetized and curarized cats. Extensor motoneurons are much less active than flexors during typical EEG seizures. Unlike the flexor neurons α and γ extensor motoneurons are activated separately, without clear temporal relation between their discharges and electrocortical symptoms. Fusimotor activity of extensors increases only after the end of the cortical seizure. Convulsive activation of α and γ extensor motoneurons is often stronger in the absence of EEG paroxysmal waves than during a seizure. These observations suggest that convulsive activity of extensor motoneurons is not directly dependent on epileptic phenomena occurring in the motor cortex and extensor activation seems more likely connected to extrapyramidal projections of the epileptic process.     

Curcumin differentially regulates the expression of superoxide dismutase in cerebral cortex and cerebellum of l-thyroxine (T4)-induced hyperthyroid rat brain

The present investigation was aimed to elucidate the effect of curcumin on lipid peroxidation (LPx) and superoxide dismutase (SOD) in l-thyroxine (T₄)-induced oxidative stress in cerebral cortex and cerebellum of rat brain. Elevated level of LPx in cerebral cortex declined to control level on supplementation of curcumin to T₄-treated rats. On the other hand, unaltered LPx level in T₄-treated rats showed a significantly decreased level of LPx on supplementation of curcumin. The increased activity of SOD and translated products of SOD1 and SOD2 in cerebral cortex of T₄-treated rats was ameliorated on supplementation of curcumin. The decreased activity of SOD and protein expression of SOD1 in cerebellum of T₄-treated rats were ameliorated on administration of curcumin. On the other hand, SOD2 expression was not influenced either by T₄-treated or by curcumin supplementation to T₄-treated rats. Results of the present investigation reveal that the regulation of expression of SOD by curcumin in different regions (cerebral cortex and cerebellum) of rat brain is different under hyperthyroidism.     

Epileptic crisis during and after cerebrovascular diseases. A clinical analysis of 78 cases]

Seventy-eight patients with post-stroke seizures were studied retrospectively to determine the clinical, EEG and CT features of these seizures and their prognosis. There were 57 cerebral infarctions and 21 hemorrhages. Twenty-eight (36%) initial seizures occurred within one month after the stroke (0-24 hours in 19 cases) and were classified as early-onset seizures. Fifty (64%) initial seizures occurred more than 3 months after the stroke (3-12 months in 33 cases) and were classified as late-onset seizures. Compared with a population of 1938 strokes admitted during the same period, the proportion of patients with alcohol abuse, infarction in the anterior cerebral artery territory, watershed infarcts and lobar haemorrhages was significantly greater in our series. The proportion did not vary with the nature of the stroke (infarction or hemorrhage), except for early onset seizures in which the proportion of hemorrhages was significantly greater. Nor did it vary with the cause of hemispheric infarctions (cardioembolism or atherothrombosis or others). Ninety-five percent of the lesions affected the cerebral cortex or the subcortical white matter or both. Of all 78 initial seizures, 64% were partial motor (simple or secondarily generalized); 32% were primarily generalized, and 4% were partial not motor; status epilepticus was seen in 14% of the cases. An initial EEG, performed in 76 patients was normal in 7. Among the remaining 69 patients EEG showed focal or diffuse slowing down in 63% and epileptic features in 37% (including 10 cases of PLEDs). Early post-seizure EEG and repeated recordings significantly increased the specificity of EEG.(ABSTRACT TRUNCATED AT 250 WORDS)     

Discharges of alpha and gamma fibers to flexor muscles during metrazol-induced seizures in cat

Efferent discharges were recorded in nerves to flexor muscles simultaneously with ECG of contralateral motor area, during metrazol-induced seizures. Coactivation of α and γ flexor motoneurons happens in convulsive phenomena related to cortical paroxysmal activity. During the tonic and clonic stages of typical seizures, there is a close temporal correlation between the discharges of the α and γ motoneurons and those of the motor cortex neurons. Convulsive manifestations which occur either without ECG symptoms, or in preparations with interrupted connections between cerebral cortex and spinal cord, follow different patterns and do not show α-γ coactivation. These observations suggest that motor cortex epileptic activity could be responsible for the flexor specific convulsive pattern, including α-γ coactivation.     

FMR1基因敲除小鼠脑组织微白蛋白表达的改变及其意义

目的 探讨微白蛋白(PV)阳性中间神经元在脆性X综合征(FXS)癫痫易感性增加中的作用. 方法 应用免疫组织化学染色检测FVB近交系雄性2、4、6 W龄FMR1基因敲除型(KO)(KO2W、KO4W、KO6W)和同龄野生型(WT)(WT2W、WT4W、WT6W)小鼠大脑纹状皮质、颞听皮质、梨状皮质及海马CA1区、CA3区、齿状回中PV的表达(n=6);应用Western blot法检测上述小鼠大脑皮层、海马组织PV的含量(n=6). 结果 KO2W、KO44W小鼠的大脑纹状皮质、颞听皮质、梨状皮质、海马CA1和CA3区PV阳性中间神经元的数量分别较WT2W、WT4-小鼠减少,差异有统计学意义(P<0.05);KO2W和KO4W小鼠大脑皮层、海马中PV含量分别较WT2W、WT4W小鼠减少,差异有统计学意义(P<0.05). 结论 PV阳性中间神经元及PV含量的减少.可能是引起FXS模型鼠癫痫易感性增加的主要原因.     

自发性高血压大鼠脑NOS亚型基因表达与SOD活性变化

目的 探讨自发性高血压大鼠（ＳＨＲ）中枢一氧化氨（ＮＯ）、超氧阴闻子改变及可能作用。方法 采用酶法及ＲＴ－ＰＣＲ等测定ＳＨＰ脑皮质超氧化物歧化酶（ＳＯＤ）、一氧化氮合酶（ＮＯＳ）活性及两种亚型（ｃＮＯＳ、ｉＮＯＳ）表达。结果 与对照组比较ＳＨＲ脑皮质ＳＯＤ活性显著增高（Ｐ〈０．０５）,ＮＯＳ活性无差异（Ｐ〉０．０５）,ｉＮＯＳ表达降低（Ｐ〈０．０１）,ｃＮＯＳ表达增高（Ｐ〈０．０５）。结论 ＮＯＳ     

Antioxidant enzymes in cerebral cortex of immature rats following experimentally-induced seizures: upregulation of mitochondrial MnSOD (SOD2)

We have recently demonstrated the evidence of oxidative stress in brain of immature rats during seizures induced by dl-homocysteic acid (dl-HCA). The aim of the present study was to investigate the antioxidant defense mechanisms under these conditions. Seizures were induced in immature 12-day-old rats by bilateral icv infusion of dl-HCA (600 nmol/side), and the activities of the main antioxidant enzymes were examined in supernatants of the cerebral cortex during the acute phase of seizures and at several periods of survival, up to 5 weeks, following these seizures. In control animals individual antioxidant enzymes revealed different changes during the studied postnatal period (PD 12 till PD 47). Total superoxide dismutase (SOD), CuZn SOD (SOD1), Mn SOD (SOD2) and glutathione peroxidase (GPX) activities were increasing while, catalase activity decreased and the activity of glutathione reductase (GR) remained unchanged. In HCA-treated animals, the activity of total SOD, SOD1 and particularly SOD2 significantly increased at 20 h and 6 days of survival. Importantly, upregulation of SOD2 was also confirmed in mitochondria at the protein level by immunoblotting. The activities of other antioxidant enzymes including catalase and GPX did not significantly differ upon HCA treatment from the appropriate controls at any of the studied time intervals. The pronounced and selective upregulation of SOD2 points to enhanced ROS levels in the mitochondrial matrix. This may be associated with inhibition of respiratory chain complex I that we have demonstrated in our previous studies. The present findings suggest that oxidative stress occurring in the brain of immature rats during and following the seizures induced by dl-HCA is apparently due to both the increased free radical production and the limited antioxidant defense.     

Oxidative metabolic responses with recurrent seizures in rat cerebral cortex: Role of systemic factors

Simultaneous focal measurements of cerebral oxygen tension and cytochrome a,a3 redox levels were made in rat cortex in order to obtain a direct and continuous assessment of oxidative metabolic changes during serial seizures. Initial seizures evoked by pentylenetetrazol were accompanied by transient increases in tissue pO2 and cytochrome a,a3 oxidation, confirming that oxygen provision is adequate to meet metabolic demand. After some point, subsequent seizures were accompanied by failure of pO2 to increase and failure of cytochrome a,a3 to oxidize, or by decreases in tissue pO2 and shifts in the redox level of cytochrome a,a3 toward reduction, signalling cortical oxygen insufficiency. Whereas early seizures were accompanied by increments in both cerebral blood volume and arterial blood pressure, one or both of these variables failed to increment during later seizures. This was particularly evident following the onset of spontaneously recurring seizures with short intervals between bursts of ECoG activity. These investigations emphasize the importance of systemic factors in determining the cerebral metabolic response to seizures and support the suggestion that neuronal damage in status epilepticus may be the result of derangements of oxidative metabolism.     

癫痫发作大鼠海马神经元凋亡与caspase-3 mRNA表达的研究

目的 :研究癫大鼠海马神经元凋亡与caspase 3mRNA表达的关系。方法 :采用大鼠红藻氨酸 (KA)致模型 ,以原位末端标记 (TUNEL)检测癫后不同时间海马神经元凋亡 ;RT PCR检测caspase 3mRNA的表达。结果 :KA致后 1d ,海马CA1、CA3及CA4区开始出现凋亡细胞 ,3d时明显增多 ,7d时最多。KA致后 6h ,海马组织caspase 3mRNA表达显著增高 ,1、3、7d仍持续高水平表达。结论 :癫大鼠海马神经元凋亡与caspase 3mRNA的表达密切相关 ,caspase 3在神经元凋亡过程中起着重要的作用