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1.
采用足底电击结合噪音制做大鼠应激模型 ,以免疫组织化学 ABC法研究了大鼠脑内 c- fos癌基因蛋白 ( FOS)在慢性应激过程中的表达情况。结果显示 ,正常对照组大鼠脑内无 FOS阳性细胞出现。而应激组大鼠脑内 FOS的表达部位随应激时间的延长而呈下降趋势 ,说明随应激时间的延长大鼠脑内不同核团神经元功能发生不同程度的障碍。大鼠的痛阈在应激后 3,9d无明显变化而在第 1 5天大鼠痛阈明显升高 ,说明长时间的电刺激产生了镇痛。  相似文献   

2.
采用足底电击结合噪音制做大鼠应激模型,以免疫组织化学ABC法研究了大鼠脑内c-fos癌基因蛋白在蛋性应激过程中的表达情况。结果显示,正常对照组大鼠脑内无FOS阳性细胞出现。  相似文献   

3.
噪音刺激下c—fos癌基因表达及钙拮抗剂防护作用的研究   总被引:5,自引:0,他引:5  
应用机能定位的形态学方法——c-fos癌基因表达法,对心理应激进行探讨。方法用86dB噪音持续刺激SD大鼠1~2小时,并与受到40dB强度生理性声音刺激和不给声音刺激的大鼠进行对比。结果接受噪音刺激的动物的脑干听觉通路各级神经元以及与情绪有关的边缘系统皮质下部位的杏仁核和下丘脑室旁核(PVN)、视上核等处出现了明显的c-fos癌基因表达产物Fos蛋白的聚集。用药与不用药组差异显著(P<0.05)。结论提示了心理应激的解剖基础和发病机制。  相似文献   

4.
偏头痛患者的屈反射阈及痛阈量化测定   总被引:1,自引:0,他引:1  
《卒中与神经疾病》1996,3(2):88-89,92
  相似文献   

5.
目的 观察旋转恒磁场不同作用时间及不同角速度对大鼠甩尾痛阈及机械缩足痛闲(MWT)的影响.方法 实验一:将48只雌性SD大鼠按照随机数字表法分为8组,根据测试时间点的不同分别定为处理前组(对照组),处理后10、20、30、60min组和处理60min停后10、20、30min组,每组6只.以恒定转速(7300 r/min)旋转磁场处理大鼠腰椎,于相应时间点分别测定大鼠甩尾反射潜伏期(TFL)及MWT,并对结果进行统计学分析.实验二:将40只雌性大鼠按照随机数字表法分为4组,每组10只.分别测定6300 r/min、6800 r/min、7300 r/min、7800 r/min不同角速度的旋转磁场处理大鼠30 min后的TFL及MWT,对结果进行统计学分析.结果 实验一:与对照组相比,大鼠经旋转磁场处理后10、20、30、60min后TFL均有明显提高,差异均有统计学意义(P<0.05);停止转动后TFL开始缩短.停后10、20 min与对照组比较差异均有统计学意义(P<0.05).大鼠MWT则于处理后30、60 min及停后10 min较对照组有明显提高,差异均有统计学意义(P<0.05).停后30min恢复至处理前水平.实验二:TFL随着转速的提高而延长,6300 r/min组、6800 r/min组与7300r/min组、7800 r/min组比较,差异均有统计学意义(P<0.05).7800 r/min组与6300 r/min组MWT比较筹异有统计学意义(P<0.05).结论 旋转磁场处理一定时间后可提升大鼠痛阈,停止处理后阈值的升高有短暂的后效应.在一定范围内痛阈随转速的升高而升高.旋磁镇痛可能成为无创镇痛的新方法.  相似文献   

6.
目的动态研究不同灌注时间和灌注量对全脑组织缺血损害的恢复程度和即早基因。c-fos的表达,以探明适应性再灌注的脑保护作用机制。方法沙鼠随机分7组,实验组夹闭两侧颈总动脉,造成沙土鼠全脑缺血模型,夹闭10 min后,不同开放时问段(4 min,8 min,10 min,15 min,30 min),开放不同脑血流量(1/ 4,1/2,一次性全开放)和单纯血液稀释后分别观察缺血海马CA区c-fos蛋白的表达,及缺血区大脑半球的改善状况。结果开放15 min,1/2脑血流量时c-fos蛋白表达最高(P<0.05),海马CA区缺血损害改善最明显,开放15 min,全脑血流量一次性开放时海马CA区损害最严重。结论(1)在适应性灌注流量中,脑缺血海马区c-fos的表达和神经元凋亡呈反相作用关系;(2)低流量灌注有明显改善脑缺血的作用,夹闭10min后, 开放1/2脑血流量,持续15 min的效果比一次性再灌注开放效果要好。  相似文献   

7.
鞘内注射曲马多对手术致痛大鼠脊髓c-fos蛋白表达的影响   总被引:1,自引:0,他引:1  
目的在大鼠手术致痛模型中研究鞘内注射曲马多对脊髓c-fos蛋白的影响,探讨曲马多的超前镇痛效应。方法选取鞘内置管成功的32只雄性大鼠随机分为4组,每组8只,分别为假手术组(S组),实验对照组(EC组),术前曲马多组(TP20组,20μg/10μl)以及术后曲马多组(PT20组,20μg/10μl)。按照Brennan法制成大鼠切口痛模型,致痛2 h后,深麻醉大鼠,灌注固定,取脊髓L4~L6节段做c-fos免疫组化染色,观察大鼠脊髓c-fos蛋白表达的变化情况。结果 3个实验组的IOD值与假手术组相比较,均有不同程度的升高,差异有统计学意义(P0.05);TP20组、PT20组的IOD值与EC组相比较,均弱于实验对照组,差异有统计学意义(P0.05);TP20组的IOD值与PT20组相比较,差异有统计学意义(P0.05)。结论手术致痛前或后,鞘内注射曲马多均能抑制大鼠脊髓背角c-fos蛋白的表达;曲马多预先给药,抗伤害作用更好,具有超前镇痛效应。  相似文献   

8.
目的:探讨雌激素对脑卒中后抑郁(PSD)大鼠蓝斑c-fos基因表达的影响,以期揭示雌激素在PSD的中枢调控机制。方法:雌性SD大鼠30只,经Open-Field行为学评分随机分成对照组、PSD组和雌激素治疗组,所有大鼠均行卵巢切除术(去卵巢)。对照组为常规喂养;PSD组去卵巢后7d,采用线栓法制备局灶性脑缺血并结合孤养、束缚应激制成PSD大鼠模型;雌激素治疗组对去卵巢后的PSD大鼠模型皮下包埋雌激素释放管(17β-雌二醇维持在生理浓度)。观察雌激素对PSD大鼠自发性行为和蓝斑c-fos表达的改变。结果:与对照组比较,PSD大鼠旷场实验中水平和垂直得分明显减少,蓝斑c-fos表达明显增加。与PSD组比较,雌激素治疗组能增加大鼠在旷场实验中得分,蓝斑c-fos表达减少。结论:雌激素对PSD大鼠的脑保护作用可能与下调c-fos基因表达有关。  相似文献   

9.
目的探讨脑出血并应激性溃疡患者血浆Ghrelin水平的变化,并分析其意义。方法收集的急性脑出血病例97例作为观察组,将其分为单纯脑出血组53例,脑出血并溃疡组44例(其中基底节42例,小脑7例,脑干12例,丘脑2例,破入脑室18例,脑叶16例),同时取30例健康体格检查者作为对照组。分别取观察组患者入院后24h内血浆,检测Ghrelin含量,进一步分析血浆Ghrelin含量、脑出血及应激性溃疡的关系。结果单纯脑出血组血浆Ghrelin水平为(166.50±74.79)μg/L,脑出血并应激性溃疡组血浆Ghrelin水平为(322.50±22.53)μg/L,对照组为(68.64±16.28)μg/L,3组比较差异有统计学意义(P<0.05)。结论急性脑出血患者血浆Ghrelin水平对诊断应激性溃疡及估计病情预后有一定提示作用。  相似文献   

10.
目的 研究健康正常人催眠静息状态和清醒安静状态痛阈差异,以及催眠敏感性与痛阈和痛阈变化的相关性。方法 用痛阈测试仪分别测定清醒安静状态和催眠静息状态的痛阈,比较两者的差异;用斯坦福敏感性量表C式测试受使者的敏感性。结果 催眠静息状态的痛阈明显高于清醒安静状态的痛阈(P=0.018);催眠敏感性与催眠静息状态痛阈和痛阌变化成正相关(P〈0.01)。结论 催眠静息状态时的痛阈明显提高,痛阈增高可以作为催眠状态界定的一个客观指标。  相似文献   

11.
Pain and severe pain thresholds were measured in groups of 15 (Experiment 1) and 20 (Experiment 2) normal volunteers. In Experiment 1, the subjects underwent a series of ten constant level, painful stimuli each of 10 sec duration at an arbitrarily chosen level between the thresholds. This level was recorded. It ranged from 14% to 81% of the difference between thresholds. The thresholds were then remeasured. For the second experiment the experimental stimulus commenced at a non-painful level and increased over a period of 5 sec to a level midway between thresholds for a series of three stimuli and again thresholds were remeasured. An overall effect was demonstrable only in Experiment 2, where the severe pain threshold was significantly reduced (p less than 0.001). There was a marked individual variation with increases and decreases in both thresholds occurring in different individuals at significance levels varying from p less than 0.05 to p less than 0.001. No subject changed the two thresholds in opposite directions. Examination of the responses in Experiment 1 suggested that for any increase in either threshold to occur it was necessary that the repeated painful stimulus should be at a level below the mid-point between the two thresholds, but that this was not a sufficient condition.  相似文献   

12.
Neonatal administration of monosodium glutamate (MSG) results in a number of anatomical, physiological and behavioral abnormalities, including changes in pain thresholds and analgesic responses. The present study compared the onsets of MSG-induced changes in jump thresholds, hot-plate latencies, and body weight. At 30, 60 and 80 days of age, MSG-treated rats weighed significantly less than rats treated with either saline or hypertonic saline (HSAL), a control for possible osmolarity effects. Jump thresholds of MSG-treated rats were significantly lower than those of saline-treated rats at 80, but not at 45 days of age. In contrast, HSAL treatment decreased jump thresholds at 45, but not at 80 days of age. Hot-plate latencies of MSG-treated rats were significantly longer than saline-treated rats across the time course of testing at 21, 45 and 80 days of age. Thus, not only did MSG treatment induce differential effects upon pain thresholds, but the onsets of such changes varied as a function of the test. The implications of differential onsets of MSG-induced abnormalities are discussed.  相似文献   

13.
In our previous studies, we have shown that stress induced by early social deprivation or total isolation, increases nitric oxide synthase activity in the brain regions of laboratory animals, and possible links between this phenomenon and stress-induced psychoemotional disturbances have been discussed. In the present study, we studied the effects of chronic psychosocial stress (housing under crowding conditions for 6 weeks) on the anxiety behavior and the indices of nitrergic system and intensity of free radical-mediated processes. Stress significantly increased anxiety levels, primarily influencing the exploratory components of animal behavior. Nitric oxide synthase activity and the levels of nitric oxide stable metabolites did not differ in the cerebral cortex, hippocampus, striatum and cerebellum of the control and stressed rats. Stress moderately increased the content of lipid peroxidation products in the cerebellum, whereas the levels of protein- and nonprotein thiol groups remained unchanged. Thus, the increased anxiety level in rats subjected to a long-term crowding was not accompanied by changes in the nitrergic system in the brain.  相似文献   

14.
目的探讨慢性应激抑郁模型大鼠脑内前额叶、海马、中缝核、伏隔核5—羟色胺1A(5—HT1A)与5—羟色胺2A(5—HT2A)受体m RNA表达的变化。方法将成年雄性SD大鼠适应性喂养1w后随机分为实验组和对照组,每组10只。实验组连续28d,随机给予强迫游泳、夹尾、潮湿垫料、鼠笼倾斜、食物和水的剥夺等其中一种刺激,建立慢性轻度不可预知应激动物模型。对照组正常饲养,不予以实验性处理。采用旷场实验及糖水偏好实验评定其行为学改变;应用逆转录聚合酶链反应检测并比较两组大鼠大脑中前额叶、海马、中缝核、伏隔核5—HT1A与5—HT2A受体m RNA的表达水平。结果 1实验组5—HTl A受体m RNA表达在前额叶、海马、中缝核、伏隔核中分别为1.35±0.05、1.76±0.35、0.84±0.67、2.17±0.56,对照组分别为1.57±0.38、2.04±0.71、0.92±0.12、2.25±0.09。2组比较差异无统计学意义(P0.05);2实验组5—HT2A受体m RNA表达在前额叶、海马、中缝核、伏隔核中分别为1.24±0.80、0.37±0.75、0.34±0.14、0.45±0.41,对照组分别为1.66±0.43、2.02±0.12、1.90±0.56、1.28±0.31,2组比较在海马,中缝核,伏隔核中差异有统计学意义(P0.05)。结论 1慢性应激抑郁模型大鼠脑内前额叶、海马、中缝核、伏隔核中5—HT1A受体m RNA表达均无变化;2慢性应激抑郁模型大鼠脑内海马、中缝核、伏隔核中5—HT2A受体m RNA表达均减少;在前额叶表达无变化。  相似文献   

15.
We investigated the ultrastructural, immunohistochemical, biochemical and behavioral effects of chronic neuroinflammation in young rats produced by injection of lipopolysaccharide (LPS) into the 4th ventricle. The 37-day infusion of LPS impaired spatial memory but not object recognition ability. Electron microscopic studies of neurons within the hippocampus identified numerous paired cisternae of the rough endoplasmic reticulum (RER) and other ultrastructural changes that suggested impaired or reduced synthesis of cellular proteins within the cytoplasm. Immunohistochemical staining found numerous highly activated microglia distributed throughout the cingulate gyrus, entorhinal cortex, hippocampus and dentate gyrus. This animal model may be useful to test potential pharmacotherapies that are directed at the prevention of the cytotoxic consequences of chronic neuroinflammation associated with normal aging or Alzheimer's disease.  相似文献   

16.
目的 探讨慢性不可预知轻度刺激(CUMS)大鼠模型中枢5-羟色胺(5-HT)含量和色氨酸羟化酶-2(TPH-2)的表达变化以及抗抑郁药的影响.方法 24只大鼠被随机分成3组,每组8只,A组为对照组,不给予刺激;B组为刺激不给药组,即CUMS应激鼠;C组为刺激给药组,即CUMS应激+西酞普兰治疗组.实验为期6周,每周为大鼠称重,每3周测大鼠的糖水偏爱性,造模前后通过旷场试验评价大鼠行为,6周后对大鼠进行处死.处死后脑组织取样测定各脑区5-HT浓度及TPH-2 mRNA的表达水平.结果 经过6周干预,与A组比较,B组和C组体重明显降低(P<0.05);与A组及C组比较,B组糖水偏爱度显著降低(P<0.05),同时行为增多;B组5-HT浓度在海马中高于A组和C组,差异有统计学意义(P<0.05);在纹状体中,B组和C组5-HT浓度低于A组,差异有统计学意义(P<0.05);B组大鼠TPH2 mRNA在中缝核中表达低于A组,差异有统计学意义(P<0.05).结论 慢性应激可能引起中枢海马5-HT浓度增高及中缝核TPH-2表达降低,抗抑郁药可能引起中枢海马5-HT浓度降低,但未能影响中枢TPH-2的表达.  相似文献   

17.
目的观察阿司匹林及细菌脂多糖对大鼠应激所致的行为性抑郁影响。方法将72只SD雄性大鼠随机分为对照组和应激组。应激组大鼠在16d内接受小同类型的应激,制备应激性抑郁症模型。采用开场试验检测大鼠的行为性抑郁,用甲基噻唑基四唑比色法测定淋巴细胞转化。结果慢性应激大鼠从第7~14天出现总活动路程、总活动时间和中区活动时间减少,呈现明显的行为性抑郁。腹腔注射细菌脂多糖(100μg/kg)可加重应激引起的行为性抑郁,并加强应激大鼠血清对正常淋巴细胞转化的抑制作用,导致正常大鼠的总活动路程显著缩短。阿司匹林(50mg/kg)对正常大鼠无显著性影响,但可减轻大鼠的行为性抑郁和应激大鼠血清对正常淋巴细胞转化的抑制作用。结论腹腔注射细菌脂多糖加重应激大鼠的行为性抑郁,阿司匹林可减轻大鼠的行为性抑郁。  相似文献   

18.
百日咳菌液致脑水肿时大鼠脑组织细胞因子的变化及机制   总被引:1,自引:0,他引:1  
目的了解白细胞介素-1β(IL-1β)和肿瘤坏死因子-α(TNF-α)在感染性脑水肿(感脑)时的变化及其产生的可能机制.方法99只大鼠分成空白对照组(C组)、生理盐水组(NS组)、百日咳菌液组(PB组).NS组和PB组大鼠按注NS或PB后断头处死时间又分别分为30min、60min、120min、240min4个亚组.ELISA法测各组大鼠脑组织匀浆中的IL-1β和TNFα蛋白质水平,RT-PCR测定脑组织TNFαmRNA表达水平,电泳迁移率改变法(EMSA)检测核因子-κB(NF-κB)活性.结果注菌液后240min大鼠脑组织匀浆中的IL-1β(384.1±37.7pg/g)、TNFα(768.4±86.3pg/g)的含量明显增高,与C组、NS30min、NS60min、NS120min、NS240min及PB30min、PB60min和PB120min比较差异有非常显著性(P<0.01).RT-PCR发现TNFαmRNA表达信号在PB60min组开始增加,PB240min达高峰.NF-κB活性在PB60min组开始增加,PB120min和240min达高峰.结论脑组织中IL-1β、TNFα含量显著增加与感脑脑损害有关,其IL-1β、TNFα含量增多与NF-κB活性增加相关.  相似文献   

19.
The blood-brain barrier (BBB) is a dynamic system which maintains brain homeostasis and limits CNS penetration via interactions of transmembrane and intracellular proteins. Inflammatory pain (IP) is a condition underlying several diseases with known BBB perturbations, including stroke, Parkinson's, multiple sclerosis and Alzheimer's. Exploring the underlying pathology of chronic IP, we demonstrated alterations in BBB paracellular permeability with correlating changes in tight junction (TJ) proteins: occludin and claudin-5. The present study examines the IP-induced molecular changes leading to a loss in functional BBB integrity. IP was induced by injection of Complete Freund's Adjuvant (CFA) into the plantar surface of the right hindpaw of female Sprague-Dawley rats. Inflammation and hyperalgesia were confirmed, and BBB paracellular permeability was assessed by in situ brain perfusion of [14C]sucrose (paracellular diffusion marker). The permeability of the BBB was significantly increased at 24 and 72 h post-CFA. Analysis of the TJ proteins, which control the paracellular pathway, demonstrated decreased claudin-5 expression at 24 h, and an increase at 48 and 72 h post-injection. Occludin expression was significantly decreased 72 h post-CFA. Expression of junction adhesion molecule-1 (JAM-1) increased 48 h and decreased by 72 h post-CFA. Confocal microscopy demonstrated continuous expression of both occludin and JAM-1, each co-localizing with ZO-1. The increased claudin-5 expression was not limited to the junction. These results provide evidence that chronic IP causes dramatic alterations in specific cytoarchitectural proteins and demonstrate alterations in molecular properties during CFA, resulting in significant changes in BBB paracellular permeability.  相似文献   

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