马桑内酯致痫大鼠大脑皮层,海马谷氨酸,门冬氨酸,甘氨酸及 …

为了探讨氨基酸类神经递质在癫痫发病中的作用,我们采用高效液相色谱仪（ＨＰＬＣ）结合紫外分光光度仪分析检测了马桑内酯（ＣＬ）致痫大鼠大脑皮层、海马Ｇｌｕ、Ａｓｐ、Ｇｌｙ、ＧＡＢＡ的含量变化。结果显示：ＣＬ致痫组与正常对照组相比,Ｇｌｕ、Ａｓｐ、Ｇｌｙ含量增加（Ｐ〈０．０１,Ｐ〈０．０５）;ＧＡＢＡ含量减少,但差异无显著性（Ｐ〉０．０５）。这些结果提示兴奋性和抑制性氨基酸在癫痫发病中具有重要作用,可能     

大鼠脑缺血再灌流后海马氨基酸水平变化与神经元损害的关系探讨

目的探讨脑缺血再灌流后海马氨基酸递质变化与神经元损害的关系。方法建立大鼠前脑缺血再灌流模型,测定海马ＣＡ１区和ＣＡ３／齿状回区游离氨基酸含量,观察阻断隔－海马通路对海马神经元损害和氨基酸水平的影响。结果（１）海马结构中仅ＣＡ１区神经元明显损害,但ＣＡ１区和ＣＡ３／齿状回区的Ｇｌｕ、Ａｓｐ和ＧＡＢＡ含量无差异。（２）阻断隔－海马通路可明显减轻海马神经元损害,但对海马氨基酸水平变化无影响。结论脑缺血再灌流后,氨基酸递质水平的异常变化不是海马ＣＡ１区神经元选择性易损的唯一决定因素,隔－海马通路末梢释放的神经递质也参与海马神经元损害过程。     

大鼠全脑缺血再灌流后4个脑区的谷氨酸,门冬氨酸,甘氨酸…

应用高效液相色谱仪，紫外分光光度检测器监测，测定大鼠全脑缺血再灌流后６ｈ￣７ｄ的海马、纹状体、丘脑和新皮层组织匀浆中谷氨酸（Ｇｌｕ）、门冬氨酸（Ａｓｐ）、甘氨酸（Ｇｌｙ）和ｒ－氨基丁酸（ＧＡＢＡ）含量变化。结果显示在海马和丘脑Ｇｌｕ含量于再灌流后６ｈ￣３ｄ下降（Ｐ〈０．０５和０．０１），ＧＡＢＡ含量升高（Ｐ〈０．０５和０．０１），在纹状体和新皮层除ＧＡＢＡ外，分别于６ｈ￣５ｄ均有不同呈度的升高。比     

微波辐射对海马CA-1区神经元的损害及其防治

目的探讨低强度微波辐射对海马神经元的损害及丹参的保护作用。方法检测大鼠暴露于微波辐射后海马ＣＡ－１区组织ＡＴＰ酶活性、Ｎａ＋、Ｋ＋、Ｃａ２＋含量,并观察病理组织学的改变。结果微波辐射２４小时后海马组织Ｎａ＋－Ｋ＋－ＡＴＰ酶、Ｃａ２＋－ＡＴＰ酶活性较正常对照组明显降低（Ｐ＜０．０１）,Ｎａ＋、Ｃａ２＋含量则较对照组明显增高（Ｐ＜０．０１）。丹参治疗组海马组织ＡＴＰ酶抑制程度及Ｎａ＋、Ｃａ２＋聚积程度较辐射组显著降低（Ｐ＜０．０１）,病理学检查神经元损害也明显减轻。结论低强度微波辐射可引起海马ＣＡ－１区神经元特异性损害,丹参对此有一定保护作用。     

脑缺血选择性海马CA1区神经元损害的实验研究

采用Ｐｕｌｓｉｎｅｌｉ－Ｂｒｉｅｒｌｅｙ４血管阻塞脑缺血模型观察了大鼠全脑缺血２０ｍｉｎ再灌流８ｈ，ｃ－ｆｏｓ基因表达及再灌流７ｄ海马ＣＡ１区迟发性神经元损害。在缺血再灌流早期（８ｈ）海马ＣＡ１区极少ｃ－ｆｏｓ表达，而齿状回、海马ＣＡ３区、杏仁核大量ｃ－ｆｏｓ表达。缺血再灌流晚期（７ｄ）镀银染色显示海马ＣＡ１区神经元及其突触终末带呈黑色溃变相，而齿状回、海马ＣＡ３区、杏仁核呈金黄色正常相。相邻切片ＨＥ染色示缺血组海马ＣＡ１区核完整的锥体细胞数（５±２．６个／２００μｍ）与对照组（４０±２．９个／μｍ）比较差异有显著意义（Ｐ＜０．０１）。脑缺血诱导的ｃ－ｆｏｓ基因表达对于缺血易损海马ＣＡ１区迟发性神经元坏死可能起直接的调控作用。     

醒脑健神胶囊对大鼠脑缺血后海马迟发性神经元坏死的保护作用

近年来,大量文献报道短暂性脑缺血可导致海马ＣＡ1区神经元选择性坏死,并且海马ＣＡ1区神经元损伤是一个缓慢进行性过程,短暂性脑缺血后随着再灌流期延长,神经元损伤进一步加重,此现象称为迟发性神经元坏死(ｄｅｌａｙｅｄｎｅｕｒｏｎａｌｄｅａｔｈ,ＤＮＤ)。本实验目的在于阐明兴奋性氨基酸和Ｃａ2 在短暂性脑缺血后海马ＤＮＤ发生机制中的作用,并用醒脑健神胶囊进行治疗,以探讨其对该损伤的脑神经细胞的保护作用。资　　料实验动物　雄性ｗｉｓｔａｒ大鼠65只,体重170～200克,由解放军309医院动物中心提供。实验药品　醒脑健神胶囊:吉林…     

马桑内酯致癫痫大鼠大脑皮层及海马氨基酸含量的测定

脑内主要的兴奋性氨基酸(ＥＡＡｓ)有谷氨酸(Ｇｌｕ)和天冬氨酸(Ａｓｐ),抑制性氨基酸(ＩＡＡｓ)有γ氨基丁酸(ＧＡＢＡ)和甘氨酸(Ｇｌｙ)。我们采用高效液相色谱仪结合紫外分光光度仪检测了马桑内酯(ＣＬ)致癫痫大鼠大脑皮层、海马Ｇｌｕ、Ａｓｐ、Ｇｌｙ及ＧＡＢＡ的含量变化,探讨癫痫发作的病理生理机制。材料和方法:　雌性ＳＤ大鼠12只,体重160～180ｇ。行双侧卵巢摘除术。术后第8天将动物随机分成正常对照组(Ｎ)和ＣＬ致癫痫组(ＣＬ),每组6只。立体定位仪下行右侧侧脑室注药。Ｎ组注入生理盐水2μｌ,ＣＬ组按50μｌ/ｋｇ体重注入ＣＬ。…     

神经节苷脂对缺血性大鼠脑保护作用的研究

目的探讨神经节苷脂（ＧＭ１）的脑保护作用及其可能机制。方法用四血管闭塞（４ＶＯ）全脑缺血再灌注模型,用高效液相色谱仪柱前衍生色谱法测定假手术组、缺血３０ｍｉｎ再灌注６０ｍｉｎ生理盐水（ＮＳ）处理组、缺血３０ｍｉｎ再灌注６０ｍｉｎＧＭ１处理组的海马组织兴奋性氨基酸（ＥＡＡ）含量,并观察缺血３０ｍｉｎ再灌注４ｄ海马ＣＡ１区病理变化。结果缺血再灌注ＮＳ处理组海马组织ＥＡＡ含量显著性降低（Ｐ＜０．０１）,海马ＣＡ１区多数神经元坏死,残存神经元呈较严重缺血性改变,ＧＭ１处理组上述生化病理改变明显为轻。结论推测ＧＭ１可调控缺血再灌注早期ＥＡＡ的过度释放和（或）重摄取受阻,减轻其在细胞外堆聚引起的兴奋毒性损伤,具有脑保护作用。     

实验性犬SAH后CVS血浆、CSF中ET、CGRP含量动态变化及巴曲酶的保护作用研究

采用放免法动态观察了２５只实验性犬ＳＡＨ后ＣＶＳ动物模型的血浆、ＣＳＦ中ＥＴ及ＣＧＲＰ含量变化及巴曲酶的保护作用。结果：单纯注血组及巴曲酶治疗组的血浆、ＣＳＦ中ＥＴ含量较对照组明显增高（Ｐ＜０．０１），ＣＧＲＰ含量明显降低（Ｐ＜０．０１）。单纯注血组在注血后３０ｍｉｎ血浆、ＣＳＦ中ＥＴ含量开始升高，ＣＧＲＰ含量开始下降，至第７ｄＥＴ达最高值，ＣＧＲＰ达最低值。经蛛网膜下腔及静脉注入巴曲酶０．４ＢＵ／ｋｇ／ｄ组，血浆及ＣＳＦ中ＥＴ含量均较同期单纯注血组明显降低（Ｐ＜０．０１），而ＣＧＲＰ则明显升高（Ｐ＜０．０１）。提示血浆、ＣＳＦ中ＥＴ、ＣＧＲＰ失衡是ＳＡＨ后ＣＶＳ的原因之一。巴曲酶可防止ＥＴ升高和ＣＧＲＰ降低。     

脑梗塞患者血及脑脊液中兴奋性氨基酸递质的动态观察

目的观察脑梗塞患者血及脑脊液（ＣＳＦ）中兴奋性氨基酸浓度的动态变化，并探讨其变化规律及临床意义。方法应用高效液相色谱系统，测定了１０例正常对照组和４１例脑梗塞患者起病后７ｈ～１０ｄ的血和ＣＳＦ中谷氨酸（Ｇｌｕ）和天门冬氨酸（Ａｓｐ）浓度的变化。结果Ｇｌｕ及Ａｓｐ的浓度在２４ｈ后开始明显升高，３ｄ达高峰，５ｄ后开始下降，７ｄ后基本接近正常水平。同时发现脑梗塞后血和ＣＳＦ中Ｇｌｕ含量呈正相关。ＣＳＦ中Ｇｌｕ浓度的变化与梗塞直径、病程和神经功能评分也呈显著相关。结论Ｇｌｕ和Ａｓｐ在脑梗塞的病理过程中起着重要作用。血和ＣＳＦ中Ｇｌｕ和Ａｓｐ浓度可以作为临床观察病情变化、梗塞面积及病程演变的客观指标。     

Denervation study of synapses of organ of corti of old world monkeys

Fine structural characteristics of synapses in the spiral organ of Corti were examined, with reference to differences between inner and outer haircell systems, and to location of neurons of origin of efferent axons. Surgical interruption of crossed olivocochlear bundle, of vestibular nerve, of facial nerve, and excision of superior cervical ganglia were used to determine the pathways of efferent axons. Interruption of the vestibular nerve near the brainstem results in degeneration of all efferent terminals on outer hair cells. Mid-line lesions at, and caudal to, the facial colliculus result in degeneration of about half of these efferent terminals. Efferent synaptic bulbs to the inner hair-cell system are small, of the order of one micron, and form type 2 junctions with afferent dendrites. They tend to have more large dense-core vesicles (about 80 nm) than the large efferent terminals of the outer hair-cell system, and appear to be the terminals of axons in the habenula perforata, which exhibit varicosities laden with large dense core vesicles. The varicosities are unaffected by excision of the superior cervical ganglia. So far as our material can reveal, it appears that the varicosities in the habenula perforata do not survive vestibular root interruption, nor do the efferent processes in the internal spiral bundle or at the base of inner hair cells. Most interestingly, the afferent processes of the inner hair-cell system, as identified for example by their relation to pre-synaptic bodies in the inner hair cells, are subject to a trans-synaptic reaction after severance of the vestibular root. They undergo a dramatic cytological transformation, characterized by increase of volume, engorgement with microtubules, microfilaments, microvesicles of various sizes, and clusters of lysosomes. Thus, both the efferent and afferent terminals of the inner hair-cell system show marked cytological differences from the corresponding terminals of the outer hair cell system.     

Mechanism of action of tubocurarine on nicotinic cholinoreceptors of neurons of the sympathetic ganglia of rats

Tubocurarine (Tc) effect on membrane currents elicited by acetylcholine (ACh) was studied in isolated superior cervical ganglion neurons of rat using patch-clamp method in the whole-cell recording mode. The "use-dependent" block of ACh current by Tc was revealed in the experiments with ACh applications, indicating that Tc blocked the channels opened by ACh. Mean lifetime of Tc-open channel complex, tau, was found to be 9.8 +/- 0.5 s (n = 7) at -50 mV and 20-24 degrees C. tau exponentially increased with membrane hyperpolarization (e-fold change in tau corresponded to the membrane potential shift by 61 mV). Inhibition of the ACh-induced current by Tc (3-30 microM/1) was completely abolished by membrane depolarization to the level of 80-100 mV. Inhibition of ACh-induced current was augmented at increased ACh doses. It is concluded that the open channel block produced by Tc is likely to be the only mechanism for Tc action on nicotinic acetylcholine receptors in superior cervical ganglion neurons of rat.     

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     

Limits of deinstitutionalization--perspectives of relatives of psychiatric patients

After a hopeful beginning, the social process of the reintegration of those with severe mental illness has come to a standstill. I am led to wonder whether "the community" really wants to live together with people suffering from severe mental illness, and if so, how closely? As long as the medical treatment of mental illness provided by the general practitioners is fundamentally deficient, as they are not able to prescribe the necessary interventions--such as out-patient psychiatric nursing, and service providers in the out-patient sector are content with offering increasingly intensive forms of care for the less seriously ill at the cost of the Social Welfare System--the reintegration of those with serious mental illness remains an illusion--which is mainly to the benefit of providers of residential care in homes and hostels.