拟血管性痴呆小鼠海马CA1区细胞定量分析及电针的影响

目的：观察拟血管性痴呆小鼠海马CA₁区细胞数目变化及电针的影响。方法：复制拟血管性痴呆小鼠模型，给予电针肾俞、膈俞、百会穴和药物喜德镇治疗15 d，运用高清晰度病理图文分析系统对海马CA₁区细胞数目做定量分析。结果：模型组海马CA₁区的场数目、面数密度、面密度均显著减少，电针和药物可明显增加以上各参数，且以电针作用为优。结论：电针肾俞、膈俞、百会穴可显著抑制海马CA1区细胞坏死、脱失, 抑制其细胞数目减少，可能为针刺有效治疗血管性痴呆的作用机制之一。     

拟血管性痴呆小鼠海马CAl区细胞定量分析及电针的影响

目的：观察拟血管性痴呆小鼠海马CAl区细胞数目变化及电针的影响。方法：复制拟血管性痴呆小鼠模型，给予电针肾俞、膈俞、百会穴和药物喜德镇治疗15d，运用高清晰度病理图文分析系统对海马CAl区细胞数目做定量分析。结果：模型组海马CAl区的场数目、面数密度、面密度均显著减少，电针和药物可明显增加以上各参数，且以电针作用为优。结论：电针肾俞、膈俞、百会穴可显著抑制海马CAl区细胞坏死、脱失，抑制其细胞数目减少，可能为针刺有效治疗血管性痴呆的作用机制之一。     

银杏叶提取物对拟血管性痴呆大鼠海马CA1区的保护作用

为了观察银杏叶提取物(EGb761)对拟血管性痴呆(vascular dementia,VD)大鼠海马CA1区神经细胞的保护作用,本研究通过反复夹闭再通大鼠双侧颈总动脉,同时腹膜腔内注射硝普钠制作拟血管性痴呆大鼠模型,选出造模成功者随机分为模型组及用药组,各为30只。另以条件匹配的30只大鼠为假手术组。采用Morris水迷宫和尼氏染色方法分别观察大鼠空间学习记忆能力及海马CA1区细胞形态学改变和细胞数目。结果显示:模型组大鼠在1、2和4月不同时间点测得的Morris水迷宫逃避潜伏期(EL)均较假手术组明显延长(P<0.01),药物组EL均显著短于模型组,但仍长于假手术组(P<0.05或P<0.01);各时间点模型组海马CA1区锥体细胞及其树突丢失,但药物组锥体细胞数多于模型组。上述结果说明EGb761对海马CA1区的保护作用可能是其改善VD大鼠学习记忆障碍的重要机制。     

拟血管性痴呆小鼠模型皮层及海马细胞病理组织学动态观察

目的:观察拟血管性痴呆小鼠模型大脑皮层及海马细胞病理形态学的较长期演变。方法:复制拟血管性痴呆小鼠模型,分别于术后7d、15d、30d脑部取材,石蜡切片,HE与Nissl染色,对皮层及海马细胞病理形态学进行较长期动态观察。结果:7d模型小鼠大脑皮质变薄,部分神经细胞核固缩,局限性神经元数目减少,出现筛网状结构,胶质细胞增生,15d、30d镜下与7d基本相同。海马CA₁区细胞脱失,随时间推移逐渐加重,至术后30d,海马CA₁区细胞几乎完全脱失,胶质细胞大量增生,形成结节,CA₂、CA₃区细胞也严重脱失,呈现海马硬化。结论:海马锥体细胞的迟发性坏死是缺血性脑血管病致痴呆的病理学基础。     

大鼠血管性痴呆模型动物中海马神经元凋亡和蛋白表达的研究

目的:观察不同时点分别结扎左、右颈总动脉建立大鼠血管性痴呆模型中海马CA1区神经元凋亡和Bcl-2及Bax蛋白表达的影响,探讨其在血管性痴呆发病过程中的作用。方法:采取间隔3 d分2次结扎双侧颈总动脉建立血管性痴呆模型,术后4周用TUNEL法检测海马CA1区神经元凋亡,用免疫组织化学法检测其Bcl-2及Bax蛋白表达。结果:模型组大鼠海马CA1区可见大量凋亡神经元;模型组Bcl-2及Bax蛋白表达明显增加,与假手术组比较差异均有显著意义(P<0.05)。结论:此血管性痴呆模型大鼠中海马CA1区神经元大量凋亡丢失,可能是导致血管性痴呆的病理基础。     

血管性痴呆小鼠海马结构SS及CCK蛋白表达的改变

目的:观察血管性痴呆小鼠海马结构生长抑素(SS)和胆囊收缩素(CCK)阳性神经元的数量变化,探讨血管性痴呆的发生机制。方法:复制小鼠血管性痴呆模型,利用Y-迷宫检测血管性痴呆模型小鼠学习记忆能力,采用ABC免疫组织化学方法,研究血管性痴呆小鼠与正常小鼠海马结构SS和CCK阳性神经元数量的变化。结果:血管性痴呆小鼠比正常小鼠Y-迷宫学习记忆训练次数明显增多,差异有统计学意义;海马结构CA1区、CA3区及齿状回(DG)区SS和CCK阳性神经元的数量明显减少,差异有统计学意义。结论:血管性痴呆的发生可能与海马结构CA1区、CA3区及齿状回(DG)区SS和CCK阳性神经元的数量明显减少有关。     

血管性痴呆大鼠海马synapsinⅠ及其磷酸化水平的动态变化

目的：观察血管性痴呆大鼠海马区突触结构和突触蛋白synapsin I及其磷酸化水平的变化，探讨血管性痴呆大鼠突触传递障碍的可能机制。方法: 采用双侧颈总动脉夹闭再灌注同时腹腔注射硝普纳建立血管性痴呆模型，在15 d、1月、2月和4月等时点，电镜观察大鼠海马CA1区突触结构的病理改变，应用免疫组织化学染色法测定血管性痴呆大鼠海马synapsinⅠ及其磷酸化水平的变化。结果: 假手术组大鼠海马CA1区未见明显病理改变，突触前小泡聚集成簇，模型组突触前后膜界限不清，突触后致密物减少，突触前囊泡分布分散、聚集囊泡簇减少，并随造模时间的延长，病理改变加重；模型组大鼠海马CA1区synapsin I阳性产物表达明显减少(P<0.01)，DG区分子层无明显变化(P>0.05)；模型组大鼠海马磷酸化synapsin I（p-synapsin I）阳性细胞明显减少(P<0.01,P<0.05)，15 d和1月时点大鼠海马DG区和CA1区p-synapsin I阳性细胞表达较假手术组增强(P<0.01)，2月和4月时点CA1区p-synapsin I阳性细胞表达较假手术组减弱(P<0.01)，而DG区无明显变化(P>0.05)。结论: VD模型大鼠海马突触结构受损，突触小泡簇减少；synapsinⅠ及其磷酸化水平表达降低，突触传递前机制受损可能是VD突触传递障碍的机制之一。     

血管性痴呆大鼠海马突触结构参数的变化

目的 :观察血管性痴呆大鼠海马突触结构特点 ,探讨血管性痴呆学习记忆障碍的神经病理机制。方法 :采用永久性结扎双侧颈总动脉的方法建立血管性痴呆动物模型 ,利用Morris水迷宫和Y型电迷宫检验大鼠的学习记忆能力 ,应用透射电镜和形态计量学分析血管性痴呆大鼠海马GrayⅠ型突触的突触结构参数的变化。结果 :血管性痴呆大鼠海马CA1区GrayⅠ型突触的体积密度、面积密度、比表面和面数密度均减小 ,突触平均面积增大 ;突触界面曲率、突触间隙宽度、突触后致密物厚度均减小。结论 :永久性结扎双侧颈总动脉使大鼠海马CA1区GrayⅠ型突触数量减少和形态结构发生显著变化 ,导致学习记忆障碍     

电针对阿尔茨海默病小鼠海马神经元突触损伤及对CREB/BDNF信号通路的影响

目的探讨电针对APP/PS-1转基因小鼠海马神经元突触损伤及对CREB/BDNF信号通路的影响。方法将7月龄APP/PS-1转基因小鼠随机分为模型组、电针组及药物组,每组10只;另取10只同龄C57BL/6小鼠作为对照组。电针组针刺百合、印堂穴,并接入电针仪,20 min/次/天,共治疗15天;药物组给予盐酸多奈哌齐灌胃治疗;对照组及模型组不予以治疗。Morris水迷宫检测各组小鼠学习记忆能力;筑巢实验检测小鼠智力改变;尼式染色检测各组小鼠海马尼氏体变化;Western blot检测小鼠海马区SYN、PSD95、GAP43、CREB、pCREB及BDNF蛋白表达。结果 Morris水迷宫结果显示,与对照组相比,模型组小鼠逃避潜伏期增加,穿越平台次数减少,在目标象限停留时间减少;电针及药物组小鼠逃避潜伏期减少,穿越平台次数增加,在目标象限停留时间延长。模型组筑巢分数较对照组明显降低,电针及药物组小鼠筑巢分数明显增加。电针及药物组小鼠海马区神经元排列整齐且尼氏体数量增加,SYN、PSD95及GAP43蛋白表达增加。电针及药物组小鼠海马区pCREB及BDNF蛋白表达较模型组增加。结论电针减轻小鼠海马神经元突触损伤,改善APP/PS-1转基因小鼠的学习记忆能力,可能与调控CREB/BDNF信号通路相关蛋白表达有关。     

β-蜕皮甾酮对匹罗卡品致痫小鼠海马神经元凋亡相关基因表达的影响

目的观察β-蜕皮甾酮(20-hydroxyecdysone)对小鼠癫痫持续状态后海马神经元凋亡及凋亡相关基因的影响。方法将30只CD-1小鼠随机分成正常组、造模组、β-蜕皮甾酮治疗组。用锂-匹罗卡品腹腔注射法诱导小鼠癫痫持续状态,造模成功后72h,采用尼氏染色观察各组小鼠海马区神经元数目和形态的变化,免疫组化法和Westernblot法检测各组神经元凋亡及凋亡相关基因Bcl-2,Bax的表达。结果模型组小鼠CA1区部分细胞肿胀,锥体细胞排列紊乱,细胞形态不规则,药物治疗组较模型组细胞数目增多,细胞排列有所改善。免疫组化和Westernblot结果可见细胞凋亡因子Bax表达模型组高于正常对照组,药物治疗组低于模型组;抑制细胞凋亡因子Bcl-2表达模型组高于正常对照组,药物治疗组高于模型组。结论β-蜕皮甾酮(20-HE)可能通过降低Bax,提高Bcl-2蛋白的表达,减轻癫痫发生后对大脑的损害。     

Level of functioning of siblings and parents of probands of varying degrees of retardation

A further analysis of already published data supports the position that retardates of low ability level less frequently have retarded siblings, retarded parents, and parents low in occupational level than do retardates higher in ability level. The analysis supports the position that there are two types of retarded individuals, persons retarded as a result of gene or chromosomal anomalies, brain injury, etc., who more frequently occur in the lower-level retardate group, and persons whose retardation represents polygenic segregation, who more frequently occur in the higher-level group.     

Recovery of responsiveness of cells of lateral geniculate nucleus of rat

1. Recovery of responsiveness of single cells in lateral geniculate nucleus of rat has been determined in both P and I cells. There are three types of recovery curve among P cells; (a) early recovery, (b) early partial recovery followed by depression and then complete recovery, (c) prolonged depression followed by cyclic recovery. Type (c) is by far the commonest recovery curve. In contrast to the spike in a P cell, the synaptic potential recovers to its full amplitude in about 20 msec. All I cells exhibit similar rapid recovery curves after a prolonged depression.2. Conditioning stimuli applied to visual cortex also produce a prolonged depression in most P cells but I cells can be re-excited at short intervals from cortex. Decortication does not prevent the prolonged depression of the multineuronal response produced by optic nerve stimulation.3. A neuronal model is proposed to explain these observations. It is supposed that I cells (interneurones) are innervated by axon collaterals of the P cells (principal cells, projecting to visual cortex) and that the I cells exert an inhibitory influence on the P cells.     

Modes of Inheritance of Errors of Refraction

Eighteen families in which both parents had refractions within the range of +4·0 D to −4·0 D and axial lengths seen in emmetropia (22·3-26·0 mm) showed coefficients of correlation of the order 0·5 indicative of polygenic inheritance. Such coefficients were seen for axial length (0·407) and for the cornea (0·487), but not for the lens (which is known to be yoked to the axial length). No such coefficients were seen in 19 families in which one of the parents had axial length outside the emmetropic range (nine families with long axes and 10 with short axes).

The pattern of polygenic inheritance for emmetropia (completely correlated optical components) and errors of refraction up to 4·0 D (inadequately correlated components: correlation ametropia) follows that seen in stature and other measurable characters. In contrast the high refractive errors with their abnormal axial lengths (component ametropia) are—like the extremes in stature—pathological anomalies with monofactorial inheritance.

     

Analysis of two types of dopaminergic responses of neurons of the spinal ganglia of rats

It was established, in experiments on isolated spinal ganglia of adult rats in concluons of intracellular recording, that dopamine (1 M/liter) elicits depolarized responses in 61% of neurons, hyperpolarized in 20% of neurons, and depolarized-hyperpolarized in 19% of neurons. The depolarized responses are associated with the activation of D₁ dopamine receptors, and are governed by the shift of cAMP-dependent cation (sodium) channels to the conducting state. The hyperpolarized responses are triggered by the activation of D₂ dopamine receptors, which by means of HTP-binding protein convert the potassium channels to the conducting state. The change in the polarization of neurons with the action of dopamine influences their electrical excitability variously.Translated from Fiziologicheskii Zhurnal SSSR imeni I. M. Sechenova, Vol. 76, No. 6, pp. 739–745, June, 1990.