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1.
目的:观察低压低氧暴露对成年大鼠空间记忆及谷氨酸递质系统受体(AMPA,NMDA)的影响。方法:SD大鼠随机分成两组,对照组和低氧组(n=10),经过5天的Moriis水迷宫训练,分别接受常压和低压低氧暴露7天,再通过Morris水迷宫观察暴露后的空间记忆,western blot检测GluR1,NMDA受体表达情况。结果:水迷宫结果显示低压低氧暴露后,平均逃脱潜伏期增长,平台搜索能力下降。Western blot结果显示磷酸化的GLUR1受体和NMDA受体水平升高。结论:低压低氧暴露可诱导大鼠的空间记忆损伤,其机制可能与谷氨酸递质系统紊乱造成的兴奋性中毒有关。  相似文献   

2.
目的:探讨脑心通对急性低压低氧诱发的空间记忆功能损害及脑水肿的预防作用及机制。方法:144只小鼠随机分为6组:即常压常氧组、常压常氧给药组、模拟海拔4km组(4km组)、模拟海拔8km组(8km组)、模拟海拔4km给药组(4km给药组)、模拟海拔8km给药组(8km给药组)。比较各组实验前后及组间的Y型电迷宫测试成绩及脑组织水含量、伊文思兰(EB)含量。结果:各组实验前的Y型电迷宫训练成绩无显著差异,实验后常压常氧组、常压常氧给药组、4km组、4km给药组、8km组和8km给药组,Y型电迷宫测试成绩分别为90.00±6.32、93.33±5.16、56.67±8.16、86.67±8.16、45.00±10.49和85.00±5.48(P<0.01);常压常氧组、常压常氧给药组、4km组、4km给药组、8km组和8km给药组比较,脑组织水含量结果分别为77.79±0.27、77.66±0.23、78.42±0.18、77.81±0.18、79.04±0.33、77.94±0.42,EB含量结果分别为0.44±0.04、0.43±0.02、0.98±0.07、0.46±0.06、1.17±0.07、0.49±0...  相似文献   

3.
目的 对比分析慢性疲劳综合征小鼠与正常小鼠之间空间学习记忆功能存在的差异性。 方法 采用复合刺激法复制慢性疲劳综合征(CFS)小鼠模型,随后采用Morris水迷宫检测CFS小鼠与正常组小鼠之间空间学习记忆功能存在的差异。 结果 模型组小鼠寻找隐藏平台的潜伏期、总路程、平均游泳速度及目标象限滞留时间占总时间的百分比均显著低于正常组(P<0.05),正常组小鼠寻找隐藏平台主要采用空间搜索策略,而CFS小鼠主要采用重复环绕搜索策略。 结论 CFS小鼠的空间学习和记忆功能降低。  相似文献   

4.
目的:探讨慢性应激对不同性别小鼠空间认知能力的影响.方法:成年健康昆明小鼠32只,平均分为4组(n=8):雄性对照组和雄性应激组,雌性对照组和雌性应激组.研究采用改良的Kaz法,建立慢性应激小鼠模型,利用Morris水迷宫进行定位航行和空间搜索实验,观察不同性别的小鼠空间认知能力的改变.结果:经2周的应激处理后,在定位...  相似文献   

5.
目的探讨不同照射时间的恒定磁场作用对小鼠空间记忆形成的影响。方法应用水迷宫学习模型测定并对比4小时恒定磁场照射组、3小时恒定磁场照射组、2小时恒定磁场照射组和无磁场照射的正常对照组动物的空间记忆能力。结果水迷宫学习训练的实验表明第一个训练日中,4小时磁场处理组动物与正常对照组比较,动物到达水下平台所需时间延长,且具有显著性差异(P<0.05);3小时磁场处理组与正常对照组比较,动物到达水下平台所需时间缩短,且具有显著性差异(P<0.05);第二个训练日中,2小时或3小时磁场处理组与正常对照组比较,动物到达水下平台所需时间延长,且均具有显著性差异(P<0.05)。第三、四、五连续3个训练日中,3组磁场处理组动物到达水下平台所需的时间与正常对照组相比较均不具有显著性差异(P>0.05)。结论一定时间的磁场处理对小鼠空间记忆的形成有促进或损伤作用,究竟是促进还是损伤有可能取决于一个作用“窗口”问题。  相似文献   

6.
目的:研究高压氧(HBO)预处理对SPS暴露大学学习记忆能力及其大脑海马神经元细胞凋亡的影响.方法:48只雄性Sprague-Dawley大鼠(体重220-260 g)随机分为4组(n=12):对照(sham)组,高压氧(HBO)组,SPS组以及高压氧+SPS组.高压氧组每天1小时高压氧预处理(2.5个大气压,100%O2)连续5天;SPS组采用单次延长应激模型;高压氧+SPS组每天l小时高压氧预处理连续5天于最后一次预处理后24小时,制作SPS模型.4组大鼠于SPS暴露后72小时进行TUNEL染色,第15天经行水迷宫测试.结果:水迷宫实验中大鼠逃避潜伏期及游泳路径四组之间有明显统计差异[F0.01(3,28)=4.88>4.57,P<0.01;F0.01(3,28)=5.31>4.57,P<0.01].SPS组明显长于Sham组(P<0.01),而高压氧预处理能够逆转这种效应(P<0.01).游泳速度四组之间无明显统计差异[F0.05(3,28)=2.23<2.95,P>0.05]. SPS暴露后海马神经元细胞数量和密度明显减少,给予高压氧预处理后,神经元形态明显好转,但仍不及对照组.结论:高压氧预处理可以减少海马神经元细胞凋亡从而改善SPS暴露后大鼠认知功能障碍.  相似文献   

7.
目的:研究暴露在不同海拔高度的急性低压低氧环境中,大鼠空间学习记忆能力的变化及与海马内孤啡肽的关系.方法:采用低压舱模拟4 500 m(中度)和7 500 m(重度)两种海拨高度,Morris水迷宫训练方法和反转录多聚酶链式反应(RT-PCR)技术.结果:①海马内孤啡肽mRNA表达在急性重度低压低氧(8 h/d,连续6 d)后明显增加,然而在Morris 水迷宫训练(6 counts/d,连续6 d,定位航行潜伏期逐渐缩短)后则显著降低.②急性低压低氧后,定位航行潜伏期明显延长,而海马内孤啡肽mRNA表达较学习记忆训练组明显升高.结论:海马内孤啡肽参与急性低压低氧降低大鼠空间学习记忆的机制.  相似文献   

8.
本文旨在探讨亚硝酸钠对大鼠海马Tau蛋白、神经细丝(neurofilament,NF)磷酸化水平及空间学习记忆的影响。大鼠饮用水中溶入亚硝酸钠粉剂,连续饮用60 d(每天100 mg/kg),通过Morris水迷宫检测大鼠的空间学习记忆能力,免疫印迹和免疫组织化学检测海马Tau和NF磷酸化水平与分布、蛋白磷酸酯酶2A(protein phosphatase 2A,PP2A)催化亚单位蛋白水平与分布。结果显示:与对照组相比,连续饮用亚硝酸钠的大鼠空间学习记忆能力下降(P0.05),Tau蛋白Ser396/404和Ser199/202位点及NF的磷酸化水平明显升高(P0.05),PP2A的催化亚单位蛋白水平下调(P0.05)。结果提示,亚硝酸钠可以导致大鼠空间学习记忆能力下降,PP2A催化亚单位蛋白水平下调,PP2A活性抑制及骨架蛋白发生过度磷酸化。  相似文献   

9.
目的 :探讨磁场作用对小鼠学习记忆能力的影响。方法 :应用水迷宫学习模型测定并对比 30分钟磁场处理组、1 5分钟磁场处理组和非磁场处理的正常对照组动物的空间学习记忆能力。结果 :水迷宫学习训练的实验表明 30分钟磁场处理组与正常对照组比较 ,动物到达水下平台的时间延长 ;游程增加 ;平均游速减慢 ,且均具有显著性差异 (p <0 .0 5)。 1 5分钟磁场处理组与正常对照组比较 ,动物到达水下平台的时间延长 ,且具有显著性差异 (p <0 .0 5) ;游程和平均速度与正常对照组相比无显著性差异 (p >0 .0 5)。结论 :磁场处理 30分钟或 1 5分钟损伤小鼠的空间学习记忆能力 ,且以 30分钟的磁场处理作用较强  相似文献   

10.
Song SJ  Xu Y  Li FF  Yuan F  Zhou ZN  Zhang Y 《生理学报》2011,63(3):205-210
本研究旨在探讨慢性间歇性低压低氧(chronicintermittent hypobaric hypoxia,CIHH)对大鼠胸主动脉和肺动脉收缩功能的影响及其机制.雄性Sprague-Dawley大鼠随机分为4组:CIHH处理14天组(CIHH 14)、28天组(CIHH 28)、42天组(CIHH 42)和对照组(...  相似文献   

11.
目的:探讨间歇性低压低氧预处理对大鼠放射性肝脏损伤的保护作用及肝脏组织TNF-α、HIF-1α表达的影响。方法:将24只健康SPF级SD大鼠随机分为对照组(C)、照射组(R)、间歇性低压低氧预处理联合照射组(IHHP+R),于照射后6小时处死小鼠切取2块肝脏组织,采用HE染色观察肝脏的病理形态学变化,免疫组化检测肝脏TNF-α、HIF-1α的表达。结果:R组大鼠肝脏切片镜下可见中央静脉充血,肝窦淤血,肝细胞肿大,出现片状嗜酸样变性;IHHP+R组大鼠肝脏切片镜下可见中央静脉充血、肝窦淤血、肝细胞肿大程度均较R组减轻,未见嗜酸样变性。与C组相比,与C组相比,TNF-α在R组表达明显增高(P0.05),IHHP+R组TNF-α表达显著低于R组(P0.05)。C组和R组HIF-1α的表达比较差异无统计学意义(P0.05),但HIF-1α在IHHP+R组高表达,且显著高于R组(P0.05)。IHHP+R组TNF-α、HIF-1α表达呈负相关(r=-0.745,p=0.034)。结论:间歇性低压低氧处理可显著改善大鼠放射性肝脏损伤,可能与其提高HIF-1α的表达,进而抑制TNF-α的表达,减轻炎症反应有关。  相似文献   

12.
    
Increasing evidence supports the critical role of α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazolepropionic acid (AMPA) glutamate receptors in psychostimulant action. These receptors are regulated via a phosphorylation‐dependent mechanism in their trafficking, distribution, and function. The hippocampus is a brain structure important for learning and memory and is emerging as a critical site for processing psychostimulant effects. To determine whether the hippocampal pool of AMPA receptors is regulated by stimulants, we investigated and characterized the impact of amphetamine (AMPH) on phosphorylation of AMPA receptors in the adult rat hippocampus in vivo. We found that AMPH markedly increased phosphorylation of AMPA receptor GluA1 subunits at serine 845 (S845) in the hippocampus. The effect of AMPH was dose dependent. A single dose of AMPH induced a rapid and transient increase in S845 phosphorylation. Among different hippocampal subfields, AMPH primarily elevated S845 phosphorylation in the Cornu Ammonis area 1 and dentate gyrus. In contrast to S845, serine 831 phosphorylation of GluA1 and serine 880 phosphorylation of GluA2 were not altered by AMPH. In addition, surface expression of hippocampal GluA1 was up‐regulated, while the amount of intracellular GluA1 fraction was concurrently reduced in response to AMPH. GluA2 protein levels in either the surface or intracellular pool were insensitive to AMPH. These data demonstrate that the AMPA receptor in the hippocampus is sensitive to dopamine stimulation. Acute AMPH administration induces dose‐, time‐, site‐, and subunit‐dependent phosphorylation of AMPA receptors and facilitates surface trafficking of GluA1 AMPA receptors in hippocampal neurons in vivo.

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13.
The purpose of this study was to compare the effects of continuous and intermittent exercise training on serum testosterone [T] and corticosterone concentrations [Cort] during normoxia and hypobaric hypoxia. Male rats swam with loads of 3% (normoxia) or 2.25% (462 mmHg) body mass for 60 min in the continuous training groups, and 15 min separated by a 7-min rest  × 4, with 60-min total exercise duration in the intermittent training groups, 5␣days · week−1 for 6 weeks. Serum [T] were measured at␣rest and following exercise after 6 weeks of training. Serum [Cort] were measured immediately after an acute period of exercise or after 6 weeks of training at rest and following exercise. Continuous exercise induced decreases in [T] under both conditions. Intermittent exercise showed a tendency to increase [T] during normoxia, but caused a suppression during hypobaric hypoxia. The [Cort] was elevated by a similar margin after an acute period of exercise during both conditions. After 6 weeks of training, however, [Cort] increased slightly after exercise during normoxia. A lower resting [Cort], which was increased after exercise, was found in the training groups during hypoxia. No relevant relationship was found between the behaviours of [T] and [Cort] after exercise during either conditions. Accepted: 20 April 1998  相似文献   

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本研究旨在探讨并比较慢性间歇性低压低氧(intermitten thypobaric hypoxia,IHH)和慢性连续性低压低氧(continuous hypobaric hypoxia,CHH)对大鼠血液动力学作用的影响。40只成年Sprague—Dawley大鼠随机分为5组:对照组(CON),28天IHH处理组(IHH28),42天IHH处理组(IHH42),28天CHH组(CHH28)和42天CHH组(CHH42)。IHH火鼠于低压氧舱分别接受28或42天模拟5000m海拔高度低氧(11.1%O2)处理、每天6h。CHH处理大鼠生活在低压氧舱环境中,除每天半小时常氧供食、供水和清洁外,其余时间均分别接受时程为28或42天的模拟5000m海拔高度低氧(11.1%O2)处理。每周定时测定大鼠体重。通过导管法测定基础常氧和急性低氧状态下的血液动力学,包括半均动脉压(meanartery blood pressure,MAP)、心率(heartrate,HR)、左审收缩峰压(1eft ventricular systolic pressure,LVSP)、正负左率最人压力变化速率(maximum change rate of left ventricular pressure,&#177;LVdP/dtmax)。通过生物化学方法测定大鼠心肌超氧化物岐化酶活性和丙二醛含量。并分别测定全心、左心室和右心室重量。结果显示:(1)CHH42大鼠基础HR和MAP低于CON,IHH和CHH28大鼠(P〈0.05)。(2)IHH大鼠表现出明显的抗心肌缺氧/复氧损伤作用,表现为急性低氧状态下的HR、MAP、LVSP和+LVdP/dtmax,改变明显低于CON大鼠(P〈0.05);CHH大鼠表现出更为明显的抗急性低氧心脏保护作用,表现为急性低氧的HR、MAP、LVSP和&#177;LVdP/dtmax;改变明显低于CON和IHH火鼠(P〈0.05),但出现复氧损伤作用,表现为复氧过程中血液动力学的恢复明显低于CON和IHH大鼠(P〈0.05)。(3)与CON大鼠相比较,IHH和CHH大鼠心肌抗氧化能力明显增强(P〈0.05,P〈0.01)。(4)与IHH和CON大鼠相比较,CHH大鼠表现明显的右心室肥厚(P〈0.01)。结果表明,IHH可诱导有效的心脏保护作用,而无明显的不良反应,因而具有潜在的实际应用价值。  相似文献   

16.
    
We have previously shown the presence of the glycine transporter GLYT1 in glutamatergic terminals of the rat brain. In this study we present immunohistochemical and biochemical evidence indicating that GLYT1 is expressed not only at the plasma membrane of glutamatergic neurons, but also at synaptic vesicles. Confocal microscopy, immunoblots analysis of a highly purified synaptic vesicle fraction and immunoisolation of synaptic vesicles with anti-synaptophysin antibodies strongly suggested the presence of GLYT1 in synaptic vesicles. Moreover, direct observation with the electron microscope of purified vesicles immunoreacted with anti-GLYT1 and colloidal gold demonstrated that about 40% of the small vesicles of the purified vesicle fraction contained GLYT1. Double labeling for GLYT1 and synaptophysin of this vesicular fraction revealed that more of ninety percent of them were synaptic vesicles. Moreover, a significant part of the GLYT1 containing vesicles (86%) also contained the vesicular glutamate transporter vGLUT1, suggesting a functional role of GLYT1 in a subpopulation of glutamatergic vesicles.  相似文献   

17.
    
Intermittent hypobaric hypoxia can produce a protective effect on both the nervous system and non-nervous system tissues. Intermittent hypobaric hypoxia preconditioning has been shown to protect rats from cardiac ischemia-reperfusion injury by decreasing cardiac iron levels and reactive oxygen species (ROS) production, thereby decreasing oxidative stress to achieve protection. However, the specific mechanism underlying the protective effect of hypobaric hypoxia is unclear. To shed light on this phenomenon, we subjected Sprague-Dawley rats to hypobaric hypoxic preconditioning (8 hours/day). The treatment was continued for 4 weeks. We then measured the iron content in the heart, liver, spleen, and kidney. The iron levels in all of the assessed tissues decreased significantly after hypobaric hypoxia treatment, corroborating previous results that hypobaric hypoxia may produce its protective effect by decreasing ROS production by limiting the levels of catalytic iron in the tissue. We next assessed the expression levels of several proteins involved in iron metabolism (transferrin receptor, L-ferritin, and ferroportin1 [FPN1]). The increased transferrin receptor and decreased L-ferritin levels after hypobaric hypoxia were indicative of a low-iron phenotype, while FPN1 levels remained unchanged. We also examined hepcidin, transmembrane serine proteases 6 (TMPRSS6), erythroferrone (ERFE), and erythropoietin (EPO) levels, all of which play a role in the regulation of systemic iron metabolism. The expression of hepcidin decreased significantly after hypobaric hypoxia treatment, whereas the expression of TMPRSS6 and ERFE and EPO increased sharply. Finally, we measured serum iron and total iron binding capacity in the serum, as well as red blood cell count, mean corpuscular volume, hematocrit, red blood cell distribution width SD, and red blood cell distribution width CV. As expected, all of these values increased after the hypobaric hypoxia treatment. Taken together, our results show that hypobaric hypoxia can stimulate erythropoiesis, which systemically draws iron away from nonhematopoietic tissue through decreased hepcidin levels.  相似文献   

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We have prepared highly purified synaptic vesicles from rat brain by subjecting vesicles purified by our previous method to a further fractionation step, i.e., equilibrium centrifugation on a Ficoll gradient. Monoclonal antibodies to three membrane proteins enriched in synaptic vesicles--SV2, synaptophysin, and p65--each were able to immunoprecipitate specifically approximately 90% of the total membrane protein from Ficoll-purified synaptic vesicle preparations. Anti-SV2 precipitated 96% of protein, anti-synaptophysin 92%, and anti-p65 83%. These results demonstrate two points: (1) Ficoll-purified synaptic vesicles appear to be greater than 90% pure, i.e., less than 10% of membranes in the preparation do not carry synaptic vesicle-associated proteins. These very pure synaptic vesicles may be useful for direct biochemical analyses of mammalian synaptic vesicle composition and function. (2) SV2, synaptophysin, and p65 coexist on most rat brain synaptic vesicles. This result suggests that the functions of these proteins are common to most brain synaptic vesicles. However, if SV2, synaptophysin, or p65 is involved in synaptic vesicle dynamics, e.g., in vesicle trafficking or exocytosis, separate cellular systems are very likely required to modulate the activity of such proteins in a temporally or spatially specific manner.  相似文献   

20.
目的: 探讨模拟海拔7 000 m低压低氧环境对大鼠心脏结构和功能的影响。方法: 96只雄性SD大鼠随机分为常压常氧对照组(对照组)和高原低压低氧组(低氧组)。低氧组大鼠放置于大型多因素复合环境模拟实验舱内,模拟海拔7 000 m高原环境饲养。实验舱运行时间23 h/d,控制昼夜比大约12 h∶12 h;对照组置于相同条件的常压常氧环境下饲养。低氧组又根据低氧时间不同分为3 d组、7 d组、14 d组和28 d组,同时设置与各低氧组相对应的对照组,每组均12只大鼠。应用超声心动图、心电图、血常规、血生化综合评价高原低压低氧环境下大鼠心脏结构和功能变化,心肌组织HE染色分析心肌组织病理变化。结果: 与相同时间点对照组比较①随着低压低氧暴露时间延长,大鼠体质量增长明显缓慢,动脉血氧饱和度14 d和28 d显著降低(P<0.05)。②低氧组大鼠左心室舒张末期前壁厚度(LVAWD)及左心室舒张末期后壁厚度(LVPWD)于28 d时显著升高(P<0.05)。舒张末期左心室腔直径(LVIDD)及收缩末期左心室腔直径(LVIDS)于28 d时明显降低(P<0.05,P<0.01)。左心室射血分数(EF%)、左室短轴缩短率(FS%)、肺静脉血流峰值速度(PV peak velocity)及肺静脉血流峰梯度(PV peak gradient)于低氧7 d 下降明显(P<0.05,P<0.01),低氧14 d 及低氧28 d 恢复。③低氧组大鼠心电图QRS间期与QT间期在14 d 及28 d 显著延长(P<0.05,P<0.01)。ST段3 d和7 d显著压低(P<0.05,P<0.01)。R波振幅于 7 d、14 d 及28 d 显著降低(P<0.05,P<0.01)。④低氧各组大鼠红细胞计数(RBC)、血红蛋白(HGB)、红细胞分布宽度(RDW)均明显升高(P<0.01)。血小板计数(PLT)于14 d 及28 d 明显下降(P<0.01)。血肌酐(CR)于14 d及28 d显著升高(P<0.05)。⑤心肌病理提示,低氧3 d 和7 d 可见心肌水肿、肌浆凝聚,横纹不清,灶状变性和坏死伴炎性细胞浸润。低氧14 d 和28 d 心肌组织炎症性病理损伤逐渐减少。心肌细胞逐渐肥大,成纤维细胞逐渐增生。心肌间质胶原纤维逐渐增多等心肌代偿修复性病理变化显著。结论: 暴露于模拟海拔7 000 m低压低氧环境下3 d大鼠心功能明显降低,7 d最为显著。  相似文献   

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