电针对拟老年性痴呆大鼠学习记忆和海马神经元突触形态可塑性的影响研究

目的探讨电针对拟老年性痴呆大鼠学习记忆功能和海马CA1区突触可塑性的影响。方法采用腹腔注射D-半乳糖、东莨菪碱,胃饲三氯化铝（AlCl3）制备多因素损伤拟老年性痴呆动物模型,在造模同时给予电针干预,穴位选择为百会、大椎、肾俞、足三里。应用跳台实验检测大鼠学习和记忆能力,透射电镜测定突触面数密度、面积密度和体积密度变化。结果跳台实验（潜伏期、错误次数）提示,与空白对照组比较,模型组大鼠出现明显的学习记忆功能障碍,潜伏期缩短,错误次数增加（P〈0．01）。与模型组比较,电针治疗能够改善大鼠的学习和记忆功能,延长潜伏期和减少错误次数（P〈0．05,P〈0．01）。与空白组比较,模型组大鼠海马CA1区突触面数密度、面积密度和体积密度均减小（P〈0．05）;模型电针组大鼠海马CA1区突触面数密度、面积密度和体积密度均有所增大（P〈0．05）。结论电针可以改善拟AD鼠的学习记忆功能,机制可能为电针促进突触可塑性发挥的作用。     

吗啡戒断后焦虑症状大鼠伏核和杏仁核突触结构可塑性

目的 探讨吗啡依赖戒断焦虑行为与大鼠伏核、杏仁核突触形态结构可塑性变化之间的相关性.方法 采用剂量递增法建立大鼠吗啡依赖模型,应用高架十字迷宫检测焦虑行为,应用透射电镜技术结合图像分析系统比较对照组、模型组和治疗组(每组均6只)大鼠伏核、杏仁核突触体视学、界面结构参数的数据.结果 (1)行为学:模型组开放臂的次数和时间均少于对照组和治疗组(P＜0.01或P＜0.05).(2)突触体视学:伏核模型组数密度(Nv)[(1.012±0.036)个/μm3]较对照组[(0.701±0.138)个/μm3]和治疗组[(0.751±0.245)个/μm3]增加(P＜0.01),面密度(Sv)和突触连接带平均面积(S)3组间比较差异无统计学意义;杏仁核模型组Nv[(0.427±0.178)个/μm3]较对照组[(0.247±0.117)个/μm3]和治疗组[(0.246±0.116)个/μm3]增加(P＜0.01或P＜0.05),模型组Sv[(0.047±0.018)μm2/μm3]较对照组[(0.030±0.012)μm2/μm3]和治疗组[(0.030±0.015)μm2/μm3]增加(P＜0.01),模型组S[(0.124±0.066)μm2]较对照组[(0.157±0.119)μm2]和治疗组[(0.159±0.114)μm2]减小(P＜0.05).(3)突触界面结构:伏核和杏仁核各自突触的突触后致密物厚度、突触活性区长度、突触间隙宽度和突触界面曲率在模型组、对照组和治疗组间比较差异均无统计学意义.结论 吗啡依赖戒断所产生的焦虑与伏核和杏仁核突触形态结构可塑性的改变有一定相关性.

Abstract：

Objective The possible correlations between morphological contracture and plastic variability of synaptic structure in nucleus accumbens and amygdala neurons were surveyed in anxious symptom rats suffered from morphine withdrawal. Methods The escalating doses of morphine and the elevated plus-maze were applied to validate anxiety-like behavior in rats. The electron microscope was applied to detect the parameters involving the synaptic stereology and structural plasticity of synaptic interface structure of the nucleus accumbens and amygdala neurons in the control group, the morphine-withdrawal group and the cured group ( n = 6 ), associated with the stereological ways. Results ( 1 ) Compared with the control group and the cured group, reductions of frequency and time of open-arm were observed in the morphine-withdrawal group ( P ＜ 0. 01 or P ＜ 0. 05 ). ( 2 ) Higher numerical density ( Nv ) [( 1. 012 ±0. 036 )/μm3] of synapses of nucleus accumbens was detected in the anxious rats ( P ＜ 0. 01 ) than in the controls [( 0. 701 ±0. 138 )/μm3] and the cured rats [( 0. 751 ±0. 254 )/μm3] . No significant difference between the surface density ( Sv ) and the mean profile area ( S ) of synapse of the nucleus accumbens was discovered. Compared with the control group [( 0. 247 ± 0. 117 )/μm3] and the cured one [( 0. 246 ±0. 116 )/μm3] , higher values of Nv [( 0. 427 ±0. 178 )/μm3] in amygdala were detected in anxious rats ( P＜0.01 or P＜0.05 ). Similarly, higher score of Sv [( 0.047 ±0.018 )μm2/μm3] in amygdala was observed in the anxious rats ( P ＜ 0. 01 ) than those of the control group [( 0. 030 ±0. 012 )μm2/μm3] and cured group [( 0. 030 ±0. 015 )μm2/μm3] . However, anxious rats [( 0. 124 ±0. 066 )μm2] appear to be lower S of synapse in amygdale ( P ＜ 0. 05 ) than those of the control group [( 0. 157 ±0. 119 )μm2] and the cured group [( 0. 159 ±0. 114 )μm2] . ( 3 )No significant difference among postsynaptic density, length of synaptic thickening, widths in synaptic interface structure on junctions and curvature of synaptic cleft region was detected in the nucleus accumbens and amygdala neurons. Conclusion In the present study, the results suggest that anxious rats suffered from morphine withdrawal could possibly be related to the plastic variability of synaptic morphological structure in nucleus accumbens and amygdale.     

癫癎大鼠海马区囊泡锚定蛋白Ⅰ的表达及突触超微结构的改变

目的 观察大鼠癫痢发作后海马区囊泡锚定蛋白Ⅰ（synapsinⅠ）的表达和突触超微结构的变化，探讨突触功能、形态可塑性与癫痢的关系。方法用锂-匹罗卡品制作癫痫大鼠模型，应用免疫组化法观察致痢后急性期、静止期和慢性期synapsinⅠ在海马的表达；应用电镜和图像处理软件观察海马突触超微结构。结果 癫痢组大鼠海马区synapsinⅠ的表达于致痢后3h减弱；6h和12h达高峰。与对照组比较差异有显著性（P〈0．05-0．01）；24h恢复正常并持续到60d。致痢后3h突触后致密物质厚度（PSD）和突触数密度（Nv）无显著改变；6hPSD增高。Nv降低；7d、30dPSD恢复正常，Nv增高。结论 synapsinⅠ的高表达和PSD的增高可能与急性期癫痢持续状态的维持有关；synapsinⅠ的正常表达和PSD的正常可能是静止期内癫痢不发作的原因之一；慢性期Nv的增加是自发性发作出现的物质基础。     

癫大鼠海马区囊泡锚定蛋白Ⅰ的表达及突触超微结构的改变

目的观察大鼠癫发作后海马区囊泡锚定蛋白Ⅰ(synapsinⅠ)的表达和突触超微结构的变化,探讨突触功能、形态可塑性与癫的关系。方法用锂匹罗卡品制作癫疒间大鼠模型,应用免疫组化法观察致疒间后急性期、静止期和慢性期synapsinⅠ在海马的表达;应用电镜和图像处理软件观察海马突触超微结构。结果癫疒间组大鼠海马区synapsinⅠ的表达于致疒间后3h减弱;6h和12h达高峰,与对照组比较差异有显著性(P<0.05～0.01);24h恢复正常并持续到60d。致疒间后3h突触后致密物质厚度(PSD)和突触数密度(Nv)无显著改变;6hPSD增高,Nv降低;7d、30dPSD恢复正常,Nv增高。结论synapsinⅠ的高表达和PSD的增高可能与急性期癫疒间持续状态的维持有关;synapsinⅠ的正常表达和PSD的正常可能是静止期内癫疒间不发作的原因之一;慢性期Nv的增加是自发性发作出现的物质基础。     

癫癎大鼠海马区囊泡锚定蛋白Ⅰ的表达及突触超微结构的改变

目的观察大鼠癫癎发作后海马区囊泡锚定蛋白Ⅰ(synapsinⅠ)的表达和突触超微结构的变化,探讨突触功能、形态可塑性与癫癎的关系.方法　用锂-匹罗卡品制作癫癎大鼠模型,应用免疫组化法观察致癎后急性期、静止期和慢性期synapsinⅠ在海马的表达;应用电镜和图像处理软件观察海马突触超微结构.结果癫癎组大鼠海马区synapsinⅠ的表达于致癎后3 h减弱;6 h和12 h达高峰,与对照组比较差异有显著性(P<0.05～0.01);24 h恢复正常并持续到60 d.致癎后3 h突触后致密物质厚度(PSD)和突触数密度(Nv)无显著改变;6 h PSD增高,Nv降低;7 d、30 d PSD恢复正常,Nv增高.结论synapsinⅠ的高表达和PSD的增高可能与急性期癫癎持续状态的维持有关;synapsinⅠ的正常表达和PSD的正常可能是静止期内癫癎不发作的原因之一;慢性期Nv的增加是自发性发作出现的物质基础.     

电针后血管性痴呆大鼠长时程增强效应及突触素表达：与尼莫地平的比较

实验通过电针刺激血管性痴呆模型大鼠百会(DU20)、大椎(DU20),分析大鼠海马长时程增强效应及突触素表达的变化,结果表明经过电针刺激后,大鼠脑组织突触素表达增加,高频刺激后相对群峰电位潜伏期缩短、相对兴奋性突触后电位斜率和相对群峰电位幅值增大,认知能力增强,效果与尼莫地平灌胃相近。提示电针百会、大椎穴可能通过促进海马突触素的表达,增强海马突触可塑性以及加快海马神经元突触传递过程,改善血管性痴呆大鼠学习记忆能力。     

慢性应激抑郁大鼠海马CA1神经元突触可塑性研究

目的 探讨慢性轻度不可预见应激(chronic unpredictable mild stress,CUMS)抑郁模型大鼠海马CA1区神经元的突触可塑性改变.方法 将20只雄性Sprague-Dawley (SD)大鼠随机等分为CUMS组和对照组,前者连续28天每天随机接受不同的应激,对照组同样条件下饲养但不给应激,至第28天进行行为测评后处死,在日立(H7500)透射电镜下测量海马CA1神经元突触界面结构参数.结果 CUMS抑郁大鼠海马CA1神经元突触活性区长度(216.64±20.19 nm)及突触后致密物厚度(42.4±5.23 nm)显著小于对照组(321.58±12.27nm,69.6±4.77 nm),差异有统计学意义(P＜0.05),突触界面曲率及宽度与对照组差异无统计学意义(P＞0.05).结论 慢性应激性抑郁大鼠存在海马CA1区神经元突触可塑性的改变.这提示抑郁症的发病机制可能与海马神经元突触可塑性相关.     

颞叶癫痫大鼠海马CA1区突触可塑性与空间记忆能力关系的研究

目的探讨颞叶癫痫大鼠海马CA1区突触超微结构与空间记忆能力改变的关系。方法以海人酸杏仁核微量注射建立经典的雄性Wistar大鼠颞叶癫痫化学点燃模型,分别于点燃后11d、17d、21d测定大鼠的空间记忆能力,并观察第21d海马CA1区神经毡突触超微结构变化。结果颞叶癫痫大鼠空间记忆能力减低,同时伴有海马CA1区神经毡内突触数密度降低(P<0．05),突触活性区膜面积缩小(P<0．05),突触界面曲率降低(P< 0．05),比表面减小(P<0．05),突触小泡数密度降低(P<0．05)。结论颞叶癫痫大鼠海马CA1区神经毡内突触损害和活力可能是导致其空间记忆能力下降的重要机制。     

吗啡戒断性焦虑大鼠海马突触界面结构及突触素表达变化

目的 探讨吗啡依赖戒断焦虑行为与海马CA1、CA3区突触界面结构和突触素表达变化之间的相关性.方法 剂量递增法建立大鼠吗啡依赖模型,高架十字迷宫检测焦虑行为,透射电镜技术结合图像分析系统、免疫组织化学比较对照组、模型组和治疗组(各6只)大鼠海马CA1、CA3区突触界面结构和突触素(P38)的表达.结果 (1)行为学:模型组开放臂的次数和时间均少于对照组和治疗组[最小有意义差异t检验(下同),P＜0.01或P＜0.05).(2)突触界面结构:模型组CA1区突触后致密物厚度[(10.7±0.9)nm]、突触活性区长度[(45±4)am]、突触间隙宽度[(3.80±0.30)nm]和突触界面曲率(1.37±0.12)均高于对照组和治疗组(P＜0.01或P＜0.05);模型组CA3区突触后致密物厚度[(12.7±1.1)nm]、突触活性区长度[(53±8)nm]、突触间隙宽度[(3.81 ±0.59)nm]、突触界面曲率(1.39±0.30)亦均高于对照组和治疗组(P＜0.01或P＜0.05).(3)突触素表达:模型组CA1、CA3区突触素吸光度(A)值分别为(0.42±0.06)和(0.43±0.05),显著高于对照组(0.2±0.02,0.25±0.03)和治疗组(0.27±0.04,0.26±0.03).结论吗啡戒断焦虑行为与海马CA1、CA3区突触形态结构可塑性及突触素表达水平有一定的相关性.     

度洛西汀和氟西汀对抑郁模型大鼠 S100B、ERK1/2－NF－κB 表达的影响

目的：比较度洛西汀和氟西汀对抑郁模型大鼠海马 S100B、ERK1/2－NF－κB 表达的影响.方法慢性轻度不可预知应激刺激法制备54只抑郁症模型大鼠,随机分为非干预组(B 组)、度洛西汀干预组(C 组)、氟西汀干预组(D 组),各18只.另外选取18只大鼠为对照组(A 组).各组灌胃[A组和 B 组(生理盐水),C 组(度洛西汀)、D 组(氟西汀)]28 d 后,应用糖水偏爱试验和旷场试验检测大鼠行为学改变.Western blot 检测各组海马 S100B、ERK1/2和 NF－κB 的表达.结果灌胃28 d 后 B 组糖水消耗率(43±15)％显著较 A、C、D 组低[(63±11)％,(67±6)％,(61±10)％](P ＜0．05). C 和 D组大鼠干预28 d 后旷场试验水平评分、垂直运动评分与潜伏期分别为(70．66±11．53)分和(67．54±10.08)分,(20．32±8．85)分和(21．34±7．46)分,(1．0±0．4)s 和(1．1±0．3)s,与 A 组(71．19±12．08)分,(20．42±8．76)分,(1．01±0．3)s 比较,差异均无统计学意义(P ＞0．05);C、D 组与 B 组比较,水平运动评分和垂直运动评分升高,潜伏期降低.A、C、D 组大鼠海马 S100B、ERK1/2、NF－κB 表达显著高于 B组(P ＜0．05),C 和 D 组差异无统计学意义.结论度洛西汀和氟西汀均能够改善抑郁模型大鼠的行为能力及上调海马 S100B、p－ERK1/2－NFκB 表达水平,但度洛西汀和氟西汀对相关因子表达的影响无差异.     

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     

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.     

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.     

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     

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.     

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。     

Standards of instrumentation of EMG

Standardization of Electromyography (EMG) instrumentation is of particular importance to ensure high quality recordings. This consensus report on “Standards of Instrumentation of EMG” is an update and extension of the earlier IFCN Guidelines published in 1999. First, a panel of experts in different fields from different geographical distributions was invited to submit a section on their particular interest and expertise. Then, the merged document was circulated for comments and edits until a consensus emerged.The first sections in this document cover technical aspects such as instrumentation, EMG hardware and software including amplifiers and filters, digital signal analysis and instrumentation settings. Other sections cover the topics such as temporary storage, trigger and delay line, averaging, electrode types, stimulation techniques for optimal and standardised EMG examinations, and the artefacts electromyographers may face and safety rules they should follow. Finally, storage of data and databases, report generators and external communication are summarized.