慢性应激对大鼠海马CA3区锥体细胞顶树突及血清皮质酮浓度的影响

目的探讨慢性应激对大鼠海马CA3区锥体细胞结构和血清皮质酮浓度的影响。方法将20只雄性Sprague-Dawley大鼠按体质量随机分为应激组和对照组,每组10只。采用高尔基染色法及酶联免疫分析方法,观察慢性强迫游泳应激对大鼠海马CA3区锥体细胞顶树突和血清皮质酮浓度的影响。结果应激组大鼠海马CA3区锥体细胞顶树突的总长度[(112±10)μm]短于对照组[(168±34)μm],差异有统计学意义(P<0.01);一级树突直径[(9.0±1.1)μm]大于对照组[(5.7±0.9)μm],差异有统计学意义(P<0.01);血清皮质酮浓度[(13±14)μg/L]低于对照组[(30±16)μg/L],差异有统计学意义(P<0.05)。结论慢性强迫游泳可引起大鼠海马CA3区锥体细胞顶树突及血清皮质酮浓度的改变。     

慢性应激对大鼠海马CA3区锥体细胞顶树突细胞骨架的效应及其机制研究

目的 探讨慢性强迫游泳应激对大鼠海马CA3区锥体细胞顶树突细胞骨架的效应及可能的机制.方法 将16只雄性Sprague-Dawley大鼠(2月龄),随机分为对照组和应激组(强迫游泳,20 min/d,共4周),每组8只.用常规透射电镜观察两组大鼠海马CA3区锥体细胞顶树突细胞骨架,用免疫组织化学方法定量测定锥体细胞内磷酸化微管相关蛋白2(MAP2)表达水平.结果 (1)海马CA3区锥体细胞顶树突内细胞骨架的变化:对照组纵切面显示微管排列整齐、连续,呈平行状;横切面显示环状微管完整、规则,分布均匀;线粒体嵴清晰.应激组纵切面显示微管断裂,平行微管间距离变宽;横切面显示微管环不完整,单体分布不均匀;线粒体嵴模糊,偶见空泡样变性.(2)海马CA3区锥体细胞磷酸化MAP2的表达:应激组大鼠平均灰度值(145.0±4.4)低于对照组(149.3±1.8)(P＜0.05),表达的阳性细胞数[(40.36±1.36)个/视野]少于对照组[(42.73±1.56)个/视野;P＜0.01].结论 慢性强迫游泳应激可导致大鼠海马CA3区锥体细胞顶树突内细胞骨架的损害,这一效应可能通过增加磷酸化MAP2的表达实现.     

应激对大鼠海马谷氨酸、天冬氨酸和γ-氨基丁酸含量的影响

目的　探讨应激对大鼠海马谷氨酸、天冬氨酸和γ 氨基丁酸 (GABA)含量的动态影响。方法　将 72只健康雄性大鼠随机分为 5个应激暴露不同时间组和对照组 ,每组 12只。利用高效液相色谱仪 紫外检测法 ,分别于应激第 1,3,7,14和 2 8天观察应激对大鼠海马谷氨酸、天冬氨酸及GABA含量的影响。结果　应激第 1天组大鼠海马谷氨酸和天冬氨酸含量与对照组相比 ,差异无显著性 ;但GABA含量 [(2 74 7± 0 339) μmol/g]低于对照组 [(3 719± 0 5 2 8) μmol/g;P <0 0 5 ]。应激第 3,7,14和 2 8天组谷氨酸含量 [分别为 (7 818± 0 799) μmol/g ,(9 0 0 7± 0 5 2 0 ) μmol/g,(8 0 4 9± 0 733) μmol/g和 (8 12 9± 1 5 5 6 ) μmol/g]高于对照组 [(6 4 11± 0 6 38) μmol/g];天冬氨酸含量 [分别为 (2 717± 0 2 5 8)μmol/g,(2 6 96± 0 317) μmol/g,(2 82 8± 0 4 6 8) μmol/g和 (4 6 4 9± 0 6 37) μmol/g]也高于对照组 [(2 0 0 3± 0 2 71) μmol/g];均P <0 0 1。应激第 14天组和 2 8天组GABA含量 [分别为 (4 4 6 2± 0 883) μmol/g和(4 4 97± 0 85 7) μmol/g]高于对照组 (P <0 0 5～0 .0 0 1) ,应激第 3天组和 7天组的GABA含量与对照组间的差异无显著性。结论　应激第 3天开始     

海人酸致痫大鼠海马神经元凋亡研究

目的　研究大鼠癫痫发作后海马神经元凋亡的时空分布。方法　采用海人酸 (KA)诱导大鼠癫痫模型 ,以原位末端标记 (TUNEL)及透射电镜检测癫痫发作后 6h、1d、3d、7d海马神经元凋亡。结果　对照组及KA致痫后 6h组 ,海马区均未发现凋亡细胞。KA致痫后 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致痫后 1d、3d、7d ,海马CA1锥体层线性长度1mm的TUNEL阳性细胞数分别为 (6 .6 0± 3.6 9)个、(13.5 7± 5 .17)个和 (2 5 .96± 4 .87)个 ;CA3区分别为 (6 .4 8± 2 .4 5 )个、(13.89± 2 .5 2 )个和 (2 8.80± 5 .39)个 ;CA4区分别为 (4 .6 0± 1.4 5 )个、(12 .2 0± 2 .0 4 )个和 (2 5 .2 0± 5 .83)个。 3个时间组相应区域凋亡神经元数比较均存在显著性差异(P <0 .0 0 1)。透射电镜观察可见典型的凋亡细胞形态学改变。结论　凋亡参与KA致痫大鼠癫痫发作后海马神经元迟发性死亡过程。     

大鼠慢性脑缺血后海马CA_1区HCN1及p38MAPK的表达

目的探讨慢性脑缺血后大鼠海马HCN1及p38MAPK表达变化及意义。方法双侧颈总动脉永久性结扎(two vessels occlusion,2VO)制备慢性脑缺血模型,40只雄性Wistar大鼠随机分为缺血1 m组和缺血2 m组,每组均设对照组,共4组。应用Morris水迷宫、HE染色、Western blot及免疫荧光双重染色观察各组大鼠认知功能改变、海马CA1区形态学变化、HCN1和p38MAPK定位及表达情况。结果与对照组相比,大鼠缺血1 m时即出现空间学习记忆能力障碍,且缺血2 m组较1 m组更加显著,具有统计学意义(P<0.05);缺血1 m组海马CA1区可见锥体细胞变性,排列松散,个别细胞脱失,伴炎细胞浸润及胶质细胞增生;缺血2 m组海马CA1区可见锥体细胞排列紊乱,细胞脱失明显;HCN1和p38MAPK共同表达于海马CA1区锥体细胞,并且随着缺血时间的延长,海马区p38MAPK表达上调、HCN1表达下调,具有显著性差异(P<0.05)。结论慢性脑缺血导致海马CA1区神经元损伤进而影响认知功能;HCN1和p38MAPK在海马CA1区锥体细胞共同表达;随着缺血时间延长p38MAPK表达上调,HCN1表达下调,推测是慢性脑缺血大鼠认知功能损伤机制之一。     

慢性应激对大鼠海马CA3区长时程增强的影响

目的　探讨慢性应激对大鼠海马CA3区长时程增强 (LTP)的影响及机制。方法　将 34只Wistar大鼠随机分成应激组 (8只 )、应激 +盐水组 (8只 )、应激 +MK 80 1组 (8只 )及空白对照组 (1 0只 ) ,应激刺激为饮水冲突模型 ,分别于实验初和LTP检测前 1天评定大鼠情绪性行为 ,在应激 1 5天后检测大鼠强直性LTP ,测量强直后 1 ,5 ,1 0 ,30 ,60 ,90 ,1 2 0minLTP群体峰电位幅度及峰潜期。结果(1 )应激前各组情绪性行为评分的差异均无显著性 ;应激后 ,应激 +盐水组 [(4 33± 0 50 )分 ]、应激 +MK 80 1组 [(3 60± 0 55)分 ]及应激组 [(2 90± 0 74)分 ]的评分均高于对照组 [(2 0 2± 1 1 6)分 ] ,差异有显著性 (P =0 0 0 0 ) ;(2 )应激组测试刺激阈值较对照组高 (45V∶30V) ;(3)在强直后第 1 ,90min时的LTP群体峰电位变化率应激组 [分别为 (2 1 1± 58) %和 (2 4 3± 69) % ]、应激 +盐水组 [分别为 (1 69±92 ) %和 (1 82± 1 61 ) % ]低于对照组 [分别为 (30 2± 2 1 0 ) %和 (30 3± 1 4 1 ) % ]和应激 +MK 80 1组 [分别为(375± 99) %和 (489± 2 36) % ] ,差异有显著性 (P <0 0 5) ,应激 +MK 80 1组与对照组的差异无显著性 ;(4)各应激组于各时点LTP峰潜期均较对照组长 ,但差异未呈显著性。结论　慢性     

慢性应激致大鼠海马长时程增强和氨基酸类神经递质改变及苯妥英钠的效应

目的　探讨慢性应激对大鼠海马长时程增强 (LTP)和氨基酸类神经递质的影响 ,以及苯妥英钠对LTP和氨基酸神经递质改变的效应。方法　将 2 4只SD雄性大鼠随机分为对照组、应激 生理盐水 (10ml/kg)组和应激 苯妥英钠 (40mg/kg)组 ,每组 8只。采用离体海马脑片结合电生理的方法观测海马CA1区LTP的变化。以群体峰电位 (PS)的幅值和场兴奋性突触后电位 (fEPSP)的斜率作为观察LTP变化的指标。应用高效液相色谱 紫外检测法检测海马氨基酸类神经递质的含量。结果　 (1)应激 生理盐水组PS幅值和fEPSP斜率在高频串刺激后增大的幅度低于对照组和应激 苯妥英钠组 (P <0 0 5 )。 (2 )应激 生理盐水组和应激 苯妥英钠组的天冬氨酸含量 [分别为(4 74 6± 0 6 0 9) μmol/g和 (4 94 8± 0 75 1) μmol/g]高于对照组 [(2 4 2 5± 0 2 11) μmol/g ,P <0 0 1];应激 生理盐水组的谷氨酸含量 [(8 0 94± 1 0 35 ) μmol/g]高于对照组 [(6 0 16± 0 6 77) μmol/g]和应激 苯妥英钠组 [(6 970± 0 6 4 7) μmol/g];P <0 0 5 ;应激 苯妥英钠组的γ 氨基丁酸 (GABA)含量[(5 14 2± 0 6 6 2 ) μmol/g]高于对照组 [(4 2 2 9± 0 4 4 9) μmol/g]和应激 生理盐水组 [(4 2 4 9± 0 4 6 3)μmol/g],P <0 0     

人参皂甙Rb3对大鼠缺氧性损伤的脑组织神经递质γ-氨基丁酸的影响

目的观察人参皂甙Rb3对缺氧及缺氧复氧的大鼠脑组织神经递质γ氨基丁酸(GABA)的影响。方法将大鼠随机分为A、B、C、D、E5组,A、C组以低压低氧暴露制作大鼠脑缺氧模型,B、D组为缺氧复氧模型。C、D组动物分别于制模前24h、1h2次腹腔注射人参皂甙Rb3溶液;采用免疫组化法,观察各组大鼠在缺氧及缺氧复氧处理后海马CA1区GABA免疫反应阳性细胞形态及数量的变化,并与正常对照组(E组)比较。结果(1)与E组相比,A、B组大鼠海马CA1区锥体细胞层GABA阳性细胞密度下降,染色较淡,突起缺如;C、D组大鼠海马CA1区锥体细胞层GABA阳性细胞密度分别较A、B组明显升高,形态与E组相似。(2)A、B、C、D、E组大鼠海马CA1区GABA免疫反应阳性细胞数分别为7.7±2.83、10.1±2.08、30.9±2.02、33.1±4.2、16.9±1.05,A、B组明显低于E组,C、D组明显高于E组(均P<0.01)。结论人参皂甙Rb3能抑制缺氧时大鼠脑组织GABA的耗竭,促进抑制性神经递质作用,对缺氧性脑损伤具有保护作用。     

抗抑郁处理对慢性应激大鼠海马鸟苷酸结合蛋白表达的影响

目的　研究抗抑郁处理对慢性应激抑郁模型大鼠海马鸟苷酸结合蛋白 (G蛋白 )表达的影响。方法　将雄性Sprague Dawley大鼠 32只随机分为 5组 ,其中应激模型组 7只 ,阿米替林治疗组(阿米替林组 ) 7只 ,电针百会印堂穴组 (电针治疗组 ) 6只 ,电针对照点组 (电针对照组 ) 6只 ,正常对照组 (不施加应激处理 ) 6只。然后用Westernblotting方法检测各组大鼠海马 3种G蛋白亚型的含量。结果　慢性应激抑郁模型大鼠海马的Gαi、Gαq蛋白表达无明显变化 ;Gαo蛋白含量 (吸光度 )为 1 19±0 15 ,高于正常大鼠的 0 91± 0 14,P <0 0 5 ;阿米替林可使其降低至正常水平 ,而电针各组未见有明显降低作用。结论　阿米替林可能通过调节Gαo表达来发挥抗抑郁作用 ,电针百会印堂穴的抗抑郁机制可能与阿米替林不同 ,与 3种G蛋白亚型的表达无关。     

苯妥英钠对应激鼠血清和海马NO含量的影响

目的　探讨慢性应激对大鼠血清和海马一氧化氮 (nitricoxide,NO)含量的影响及苯妥英钠对它们的效应。方法　利用强迫游泳作为应激源制作慢性应激模型 ,采用硝酸还原酶法测定各组大鼠血清和海马NO的含量。结果　对照组、应激组和应激给药组之间大鼠血清NO的含量差异无显著性 ;应激组大鼠海马NO的含量 (4 70± 15 9)nmol/g显著高于对照组 (2 34± 77)nmol/ g和应激给药组(2 0 2± 89)nmol/g (P <0 .0 1) ,后两组间的差异无显著性。结论　慢性应激对大鼠血清NO含量无影响 ,但可诱导大鼠海马NO含量升高 ,苯妥英钠可以抑制慢性应激所致海马NO的过度生成。     

The effect of age of onset of PD on risk of dementia

Background Dementia occurs in the majority of patients with Parkinson’s disease (PD). Late onset of PD has been reported to be associated with a higher risk for dementia. However, age at onset (AAO) and age at baseline assessment are often correlated. The aim of this study was to explore whether AAO of PD symptoms is a risk factor for dementia independent of the general effect of age. Methods Two community-based studies of PD in New York (n = 281) and Rogaland county, Norway (n = 227) and two population-based groups of healthy elderly from New York (n = 180) and Odense, Denmark (n = 2414) were followed prospectively for 3–4 years and assessed for dementia according to DSM-IIIR. All PD and control cases underwent neurological examination and were followed with neurological and neuropsychological assessments. We used Cox proportional hazards regression based on three different time scales to explore the effect of AAO of PD on risk of dementia, adjusting for age at baseline and other demographic and clinical variables. Findings In both PD groups and in the pooled analyses, there was a significant effect of age at baseline assessment on the time to develop dementia, but there was no effect of AAO independent of age itself. Consistent with these results, there was no increased relative effect of age on the time to develop dementia in PD cases compared with controls. Interpretation This study shows that it is the general effect of age, rather than AAO that is associated with incident dementia in subjects with PD. Received in revised form: 22 December 2005     

帕金森病运动症状进展分析

目的分析帕金森病(PD)患者运动症状进展特点。方法采用PD统一评分量表(UPDRS)Ⅲ对912例PD患者进行评估。结果与病程1年的患者比较,除病程1~2年的患者外,其他病程患者的UPDRSⅢ评分、强直分、姿势或步态异常分、轴性症状总分、言语分、步态分显著升高(均P0.05),病程5~6年及14年患者的震颤分,病程5~6年、7~8年、9~13年、14年患者的运动迟缓分、姿势分显著升高(P0.05~0.01)。轴性症状进展速度高于UPDRSⅢ评分。结论 PD患者病程早期UPDRSⅢ评分进展快,震颤症状进展独立于其他症状,轴性症状评分较UPDRSⅢ更敏感地反映疾病加重趋势。     

Frequency of accumulation of filaments in adaxonal cytoplasm of Schwann cells of myelinated fibers of rat spinal roots

Summary The frequency of accumulation of 6-nm filaments in the adaxonal cytoplasm of Schwann cells in the 6th lumbar dorsal and ventral roots was evaluated in 4-, 8-, 26- and 45-week-old Sprague-Dawley rats. The frequency was higher in 4- and 8-week-old (growing) rats than in 26- and 45-week old (mature) rats, and also higher in ventral than in dorsal roots in 4-, 8- and 26-week old rats. There were no clusters on certain groups of myelinated fibers according to the size of transverse axonal area, in both the ventral and dorsal roots. Therefore, this accumulation may reflect certain functions of the adaxonal cytoplasm of Schwann cell during natural growth and maturation of the axon and myelin sheath.     

Effects of prevention of afferentation of the development of the chick optic lobe

BONDY, S. C., M. E. HARRINGTON AND C. L. ANDERSON. Effects of prevention of afferentation on the developmentof the chick optic lobe. BRAIN RES. BULL. 3(5) 411–413, 1978.—The effects of unilateral extirpation of the right optic cup of the three-day incubated chick embryo upon the rate of synthesis and the stability of DNA in the non-innervated optic lobe, have been studied. This surgical procedure prevents innervation of the optic lobe contralateral to the removed eye, while the other optic lobe is normally innervated by retinal ganglion cells of the remaining eye. At the 20th day of incubation, the DNA content of the non-innervated lobe was below that of the paired lobe receiving normal innervation. This deficiency of cell number was caused by two events; death of an excess number of neurons formed early in embryogenesis and a reduced rate of glial proliferation in the later stages of incubation.     

Function of circle of Willis

Nearly 400 years ago, Thomas Willis described the arterial ring at the base of the brain (the circle of Willis, CW) and recognized it as a compensatory system in the case of arterial occlusion. This theory is still accepted. We present several arguments that via negativa should discard the compensatory theory. (1) Current theory is anthropocentric; it ignores other species and their analog structures. (2) Arterial pathologies are diseases of old age, appearing after gene propagation. (3) According to the current theory, evolution has foresight. (4) Its commonness among animals indicates that it is probably a convergent evolutionary structure. (5) It was observed that communicating arteries are too small for effective blood flow, and (6) missing or hypoplastic in the majority of the population. We infer that CW, under physiologic conditions, serves as a passive pressure dissipating system; without considerable blood flow, pressure is transferred from the high to low pressure end, the latter being another arterial component of CW. Pressure gradient exists because pulse wave and blood flow arrive into the skull through different cerebral arteries asynchronously, due to arterial tree asymmetry. Therefore, CW and its communicating arteries protect cerebral artery and blood–brain barrier from hemodynamic stress.     

他汀类药物的使用和颅内动脉瘤破裂相关性分析

目的 探讨他汀类药物对颅内动脉瘤破裂的影响。方法 2010年3月至2014年3月收治颅内囊状动脉瘤67例,其中破裂者32例,未破裂者35例。采用多变量Logistic回归评估他汀类药物的使用和颅内动脉瘤破裂的关系。结果 破裂组术前使用他汀类药物4例（12.5%,4/32）,未破裂组16例（45.7%,16/35）。破裂组服用他汀类药物的百分比显著低于未破裂组（P<0.01）。纠正潜在的混杂干扰后（or值: 0.30,95%可信空间:0.12~="" 0.64）显示,颅内动脉瘤破裂与他汀类药物的使用呈显著负相关,也与高血清总胆固醇浓度有关。结论 本结果提示他汀类药物对颅内动脉瘤破裂有一定的预防效果。     

Impact of our understanding of the genetic aetiology of epilepsy

A genetic contribution to aetiology is estimated to be present in up to 40% of patients with epilepsy. It is useful to categorise genetic epilepsies according to the mechanisms of inheritance into Mendelian disorders, non-mendelian or ‘complex’ disorders, and chromosomal disorders. Over 200 Mendelian diseases include epilepsy as part of the phenotype, and the genes for a number of these have been identified recently. These include autosomal recessive progressive myoclonic epilepsies such as Unverricht-Lundborg disease, Lafora disease and the neuronal ceroid lipofuscinoses, and three autosomal dominant idiopathic epilepsies. The last named have been shown to arise from mutations in ion channel genes. Autosomal dominant nocturnal frontal lobe epilepsy is caused by mutations in CHRNA4, benign familial neonatal convulsions by mutations in KCNQ2 and KCNQ3, and generalised epilepsy with febrile seizures plus by mutations in SCN1B. ‘Complex’, familial epilepsies are more difficult to analyse, but evidence has been obtained for loci predisposing to juvenile myoclonic epilepsy on chromosome 6p and 15q. Lastly, the genes underlying several spike-wave epilepsies in mice have been cloned, and three of these encode sub-units of voltage-gated calcium channels. Received: 29 September 1999/Accepted: 7 December 1999     

肌萎缩侧索硬化三例误诊分析

目的掌握肌萎缩侧索硬化(ALS)的诊断标准,以便早期准确诊断,避免误诊。方法分析3例ALS患者早期被误诊的临床资料。结果 3例患者均以下肢无力发病,逐渐波及上肢或对侧肢体,脊柱MR I示颈部或腰部椎间盘突出压迫硬膜囊,手术治疗后,症状无缓解,病情仍进行性加重,经肌电图检查证实为ALS。结论临床医师应熟知ALS的诊断标准,对患者详细询问病史、认真查体和电生理检查是减少ALS误诊的关键。     

腺垂体功能减退症临床特征变化分析

目的探讨腺垂体功能减退症患者的病因结构变化及临床表现。方法回顾性分析我院2013-01—2016-12住院及门诊78例腺垂体功能减退症患者的临床资料。结果男32例(41.03%),女46例(58.97%);诊断时年龄11~89岁,平均62.5岁;鞍区占位(包括术前及术后)52例(66.67%),席汉综合征8例(10.26%),空泡蝶鞍9例(11.65%),病因不明8例(10.26%),垂体-下丘脑发育不良1例(1.28%)。首次就诊科室:纳差厌食、恶心呕吐就诊于消化内科36例(46.15%)最常见。ACTH+TSH+Gn+G激素缺乏为19例最多,占24.36%,ACTH+TSH+Gn缺乏15例,占19.23%。结论腺垂体功能减退症病因结构发生变化,发病人群、首发症状及受累激素也不同,患者女性多于男性,发病年龄偏高,症状不典型,分布于临床多个科室,其中以低钠血症为首发临床表现就诊消化内科最多。     

Modelling of movement of the lamprey: Control of oscillators

This article discusses the control methods of the central pattern generator (CPG). First a control model of the CPG is presented using 2 oscillators, and we suggest that phasic modulation to the CPG by means of phasic information is effective for controlling the phase difference between oscillators. Next, two models for controlling the CPG of a lamprey are proposed. One model describes a control system from the brain stem, in which the reticulospinal neurons control the CPG by receiving feedback signals and sending control signals to the neck region of the CPG. The other is a model for learning an localized control system to generate a desired motor pattern. By means of these models, a role of the efference copy is suggested.