急性高原应激大鼠脑组织NO、SOD及血浆皮质醇的含量变化

目的 :观察急性高原应激大鼠脑组织一氧化氮 (NO)含量和超氧化物歧化酶 (SOD)活力变化 ,探讨高原应激自由基对脑的损害作用。方法 :通过急性进入高原建立急性应激模型 ,分别取脑边缘系统大脑额叶、海马、下丘脑及中脑 ,制成脑组织匀浆 ,测定NO含量和SOD活力 ,测定血浆皮质醇含量。结果 :急性高原应激组大鼠大脑额叶、海马、下丘脑组织SOD活力明显高于对照组 (P <0 0 5 ) ,NO含量在海马、下丘脑升高明显 (P <0 0 5 ) ,血液皮质醇含量增高。结论 :在高原应激反应对脑的损害中 ,自由基细胞毒性作用可能是重要因素     

睡眠剥夺后大鼠海马生化及病理变化

目的 :观察睡眠剥夺后大鼠海马超微结构的病理变化及一氧化氮 (NO)含量、超氧化物歧化酶 (SOD)活力变化。方法 :以小平台水环境法建立大鼠睡眠剥夺模型 ,并设立大平台对照组 ,分离海马 ,电镜观察海马神经细胞超微结构变化、测定海马组织匀浆NO含量和SOD活力。结果 :睡眠剥夺组大鼠海马NO含量及SOD活力均高于大平台组和正常对照组 (P <0 0 5 )。病理形态学改变 ,光镜电镜下海马神经元减少 ,核仁碎裂、胞质内细胞器减少。结论 :睡眠剥夺可引起海马NO含量和SOD活力增高 ,并且存在病理形态学改变     

维生素C对应激大鼠脑内超氧化物歧化酶含量的影响

目的 :探讨在急性应激状态下大鼠脑内超氧化物歧化酶 (SOD)活性的变化及维生素C (VitC)对SOD改变的影响。方法 :在强迫游泳应激模型中 ,大鼠用VitC慢性给药 (腹腔内注射 0 5g·Kg- 1 ,每日一次 ,连续 7天 ) ,观察强迫游泳应激后大鼠额叶、海马、中脑和下丘脑内SOD的活性。结果 :与对照组比较 ,强迫游泳组大鼠海马内SOD活性显著性增高 (t=3 3 2 4,P <0 0 1) ,额叶、中脑和下丘脑SOD活性也显著升高 (t =2 5 3 3 ,2 3 0 3 ,2 5 89,P均 <0 0 5 )。VitC组与对照组各脑区SOD活性未见明显变化 (P均 >0 0 5 ) ;但与强迫游泳组比较 ,海马内SOD活性显著性降低 (t=3 812 ,P <0 0 1) ,额叶、中脑和下丘脑内SOD活性也显著性降低 (t=2 2 5 1,2 3 42 ,2 2 16,P均 <0 0 5 )。结论 :VitC可显著减少急性应激状态下脑内产生的自由基 ,具有神经保护作用。     

急性应激时大鼠脑内一氧化氮及一氧化氮合酶的变化

目的：探讨急性应激状态下脑内一氧化氮（NO）含量和一氧化氮合酶（NOS）活性的变化及意义。方法：采用放免法测定强迫游泳应激后1、3小时的大鼠额叶、海马、中脑和下丘脑内NO含量和NOS活性。结果：应激结束后1小时，海马和下丘脑内NO含量和NOS活性均显著增高（t分别为2．32、2．61，P均＜0．05）。应激结束后3小时，额叶、海马、中脑和下丘脑内NO含量均显著增高（t分别为3．57、4．26、3．88、4．93，P均＜0．01），NOS活性均显著性增高（t分别为2．32、2．61，P均＜0．05）。结论：急性应激状态下，各脑区的NOS活性增加，产生的NO可能介导了神经毒性作用。     

手机电磁辐射对小鼠自由基影响的研究

目的 :研究经手机电磁辐射后的小鼠血清中SOD、MDA含量的变化 ,推断手机电磁辐射可能对人体造成的早期损害。方法 :应用分光光度比色法检测手机辐射后血清SOD、MDA含量 ,并与对照组进行统计学比较 ,同时电镜下观察大脑皮层、海马、小脑超微结构的变化。结果 :实验组小鼠血清SOD低于对照组 ,有显著性差异 (P <0 .0 5 ) ,而实验组MDA含量明显高于对照组 (P <0 .0 1) ;电镜下 ,实验组大脑皮层、海马、小脑超微结构与对照组相比较没有明显改变。结论 :手机辐射使小鼠体内自由基生成增多 ,对机体细胞造成早期损伤。     

限制活动慢性应激大鼠脑组织NO、NOS含量变化的研究

慢性应激对脑海马损害已得到证实[1,2 ] 。急性应激障碍和创伤后应激障碍 (ＰＴＳＤ)表现出记忆、学习等认知障碍及行为障碍 ,可能与脑边缘系统功能受损有关。病理生理机理尚不清楚 ,氧自由基对脑细胞毒性作用可能参与发病[3 ] 。近些年来研究说明ＮＯ是体内重要的自由基 ,在中枢神经系统具有重要的生理和病理作用 ,在生理情况下参与信息传递 ,在病理情况下对神经细胞具有毒性作用。本研究通过建立应激大鼠模型 ,检测大脑额叶、海马、下丘脑组织ＮＯ含量和ＮＯＳ活力的变化 ,探讨其在应激过程中及应激障碍发病中的作用。1　材料和方法1.1　…     

急性应激时大鼠脑内环核苷酸含量的变化

目的：探讨在急性应激状态下脑内的环核苷酸的变化及意义。方法：采用放免法测定游泳应激后1、3小时的大鼠额叶、海马、中脑和下丘脑内环磷腺腺苷（cAMP)、环磷酸鸟苷（cGMP)含量。结果：应激结束后1小时，海马和下丘脑内cGMP水平均显著性增高。（t分别为2．33、2．48，P均＜0．05）。应激结束后3小时，额叶、海马、中脑和下丘脑内cAMP均显著性增高（t分别为2．49、3．03、2．75、3．34，P均＜0．05），cGMP水平均显著性增高（t分别为3．34、3．67、P均＜0．01）。结论：急性应激状态下，脑内的环核苷酸被激活，cGMP可能首先被激活。     

银杏叶提取物联合盐酸文拉法辛对抑郁大鼠海马nNOS蛋白表达及NO水平的影响

目的 :探讨抑郁症脑损伤的机制 ,研究银杏叶提取物 (EGb)及合成抗抑郁药盐酸文拉法辛(Venlafaxine)对抑郁大鼠的抗脑损伤及神经元保护作用。方法 :慢性应激建立大鼠抑郁模型。将 84只雄性大鼠分为正常对照组、抑郁模型组和不同治疗组。快速断头法处死 ,取海马后一侧进行免疫组化反应 ,观察海马CA3区nNOS蛋白的表达 ;另一侧检测NO含量 ;同时测定血清中NO含量。结果 :抑郁模型组海马nNOS表达增加 ,海马及血清中NO含量增加 ,P <0 0 1;联合用药组海马nNOS表达下降 ,海马及血清中NO含量减少 ,P <0 0 1。结论 :慢性应激增加海马nNOS表达 ;EGb有减轻神经元损伤 ,保护神经元的作用 ,其与Venlafaxine合用可能会达到对抑郁进行多靶点、多层次的治疗 ,弥补单一用药的不足。     

睡眠剥夺对大鼠一氧化氮和一氧化氮合酶的影响

目的：探讨睡眠剥夺对大鼠脑组织一氧化氮（NO）及一氧化氮合酶（NOS）影响。方法：采用小平台水环境法（Flower Pot)制作大鼠睡眠剥夺模型，采用化学法和酶法观察不同时间睡眠剥夺后大鼠额叶、海马、中脑和下丘脑NO含量及NOS活性变化。结果：与正常对照组及大平台组比较，大鼠在SD后额叶和海马的NO含量及NOS活性增高，有显著性差异（P＜0．01－0．05），其余脑区无显著性差异（P＞0．05）。随着剥夺时间的延长，额叶和海马NO含量及NOS活性增高更加明显。结论：睡眠剥夺可致NO及NOS升高，可能与其学习障碍有关，NO可能参与大鼠的睡眠调节。     

慢性应激对大鼠空间学习记忆和海马一氧化氮的影响

目的 :探讨慢性应激对大鼠空间学习记忆和海马NO的影响。方法 :采用电击足底结合噪声建立慢性应激大鼠模型 ,Morris水迷宫观察动物的学习和记忆能力 ,同时检测海马NO含量和NOS活性。结果 :慢性应激大鼠在Morris水迷宫的空间学习和记忆能力明显下降 ,海马NO含量和NOS活性 (3 87± 0 47nmol/mgpro和 10 2 64± 13 33pmol/mgpro/min)显著高于对照组大鼠 (2 76± 0 43nmol/mgpro和 78 2 5± 10 67pmol/mgpro/min)。结论 :慢性应激损害大鼠空间学习和记忆能力 ,可能与其海马内NO增多有关     

旋磁场对大鼠脏器SOD活力和NO含量的影响

目的:探讨旋磁场对大鼠肝组织、肾组织、心组织和脑组织中超氧化物歧化酶(SOD)活力和一氧化氮(NO)含量的影响.方法:用邻苯三酚法测定SOD活力;NO含量的测定采用改良的Griess法.结果:在30mT磁场中曝磁30min,大鼠肝、肾、心和脑组织中SOD活力显著高于对照组(P＜0.01或P＜0.05);大鼠肝组织和肾组织中NO含量显著高于对照组(P＜0.01);心组织NO含量高于对照组(P＜0.05);脑组织NO含量无明显变化.结论:旋磁场对大鼠脏器组织SOD活力和NO含量有一定影响.     

Intensity of Oxidative and Antioxidant Processes in the Brain of Rats with Various Behavioral Characteristics during Acute Stress

We studied the effect of acute emotional stress (1-h immobilization with simultaneous electrocutaneous stimulation) on the prooxidant-antioxidant balance in emotiogenic structures of the brain in rats with various behavioral characteristics. TBA-reactive substance content in the hypothalamus of rats remained practically unchanged after stress exposure. Opposite change in activity of antioxidant defense enzymes in this structure of the brain in behaviorally active specimens probably compensate for the possible variations in LPO during emotional stress. Activities of glutathione reductase and Cu/Zn-containing SOD in the hypothalamus of passive animals decreased under these conditions. As differentiated from active rats, emotional stress in passive specimens was accompanied by the accumulation of TBA-reactive substances in the sensorimotor cortex and amygdala. The observed increase in glutathione peroxidase activity in passive animals probably serves as a secondary compensatory reaction to LPO activation. Our results illustrate specific changes in free radical processes and antioxidant defense in emotiogenic structures of the brain in rats with various behavioral characteristics after acute stress. These changes were more pronounced in behaviorally passive specimens than in active animals. It was probably related to differences in the oxidative status of CNS in rats with various prognostic resistance to similar stress factors.     

芪参复康胶囊对大鼠睡眠剥夺后脑组织NO含量和SOD活性的影响

目的观察芪参复康胶囊对大鼠睡眠剥夺（SD）后脑组织一氧化氮（NO）含量和超氧化物歧化酶（SOD）活性的影响及行为变化,探讨芪参复康胶囊对睡眠剥夺的保护作用。方法采用小平台水环境法制作大鼠TSD模型,观察大鼠经过3天SD后额叶和海马NO含量和SOD活性,并观察采用芪参复康胶囊干预对这些指标的影响。结果与正常对照组比较,SD大鼠额叶和海马NO含量和SOD活性均升高。芪参复康胶囊干预后大鼠脑内NO含量及SOD活性明显下降（P〈0.01~0.05）。结论芪参复康胶囊具有改善生化代谢作用,可减轻睡眠剥夺对机体的损害。     

Effect of acute noise stress on acetylcholinesterase activity in discrete areas of rat brain

Effect of various stressor agents on the adrenergic system in brain had been studied extensively. However, reports on the effect of stress on various parameters of central cholinergic system are scanty. And very little is known about the effect of noise stress on the cholinergic system in brain. Hence, it was decided to elucidate the effect of acute noise stress on the activity of the enzyme acetylcholinesterase in discrete areas of brain in albino rats. Male albino rats of Wistar strain were subjected to acute noise stress for 30 minutes. The noise of pure sine wave tone was produced by using a function generator and was amplified. The frequency of noise generated was 1 kHz and the intensity was set at 100 dB. The total acetylcholinesterase activity was determined in the tissues of cerebral cortex, corpus striatum, hypothalamus and hippocampus of brain in these rats. The enzyme activity was estimated by colorimetric method using acetylthiocholine iodide as the substrate. The values were compared with the enzyme activity in the control rats. The activity of the enzyme increased significantly in all the four regions of the brain in rats after exposure to noise stress for 30 minutes. The results of the study indicate that the exposure to acute noise stress could modulate the cholinergic system in these areas of brain in rat.     

Distribution of Alzheimer's disease amyloid A4-generating enzymes in rat brain tissue

To screen for putative amyloid A4-splitting proteinases, model peptide substrates homologous to the N- and C-terminal portions of the A4 protein were synthesized. The N-terminal A4-splitting enzyme activity was found to be higher in the hypothalamus and limbic area, compared with in the cerebral cortex and cerebellum in 2-month-old rat. The activity decreased throughout the brain in 20-month-old rat. On the other hand, the activity of the putative C-terminal A4-splitting enzyme was significantly higher, 1.4-fold, in the hippocampus than in the cerebral cortex in the young rat. The activity also significantly decreased in the brain of 20-month-old rat, but was still higher in the cerebral cortex, hippocampus and cerebellum.     

Gender-specific effects of social housing on chronic stress-induced limbic Fos expression

Stress plays an important role in the development of affective disorders. Women show a higher prevalence for these disorders then men. The course of a depressive episode is thought to be positively influenced by social support. We have used a chronic mild stress model in which rats received footshocks daily for 3 weeks. Since rats are social animals we hypothesised that social housing, as a possible model for human social support, might reduce the adverse effects of chronic stress. Brain activity after chronic stress was measured in several limbic brain areas with the neuronal activation marker c-fos. High behavioural activity due to housing rats under reversed light-dark conditions could be responsible for the observed high within group variability in some limbic regions. FOS- (ir) in the paraventricular nucleus of the hypothalamus (PVN) was increased in all stress-exposed groups, except for the socially housed females who showed increased FOS-ir in control condition. Individually housed males and socially housed females showed increased FOS-ir in the dorsal raphe (DRN). Amygdala nuclei were differentially affected by stress, gender and housing conditions. Also the mesolimbic dopaminergic system showed gender specific responses to stress and housing conditions. These results indicate that social support can enhance stress coping in female rats, whereas in males rats, group housing appears to increase the adverse effects of chronic stress, although the neurobiological mechanism is not simply a reduction or enhancement of stress-induced brain activation.