针刺抗脑缺血性神经元凋亡作用与机制的研究

本研究在肯定针刺抗缺血性神经元凋亡的基础上,进一步探讨针刺对内源性促凋亡因素及抑制凋亡因素的调整作用,寻找针刺对元保护作用的切入点及作用机制。结果表明：（１）针刺能减轻脑缺血导致的神经缺损行为异常,缩小梗塞面积;（２）ＰＩ荧光染色及ＴＵＮＥＬ染以显示：大鼠缺血皮层梗塞区有大量凋亡阳性信号细胞,电针后细胞凋亡受到明显抑制测定ＮＯ含量及观察ｃＮＯＳ和ｉＮＯＳ免疫活性显示：大鼠脑缺血－再灌注后脑内ＮＯ水     

动脉粥样硬化易损斑块的分子影像研究进展

动脉粥样硬化是心脑血管疾病最主要的病因,而其中易损斑块的突然破损所诱发的血小板聚集和血栓形成是引起脑卒中和急性心肌梗死的重要发病机制.如何更有效地早期诊断动脉粥样硬化的易损斑块是目前研究的热点.文章主要就近年来分子影像技术用于动脉粥样硬化易损斑块的评价研究进行综述.     

冠状动脉易损斑块影像学最新研究进展

冠心病(CAD)是世界上致死率最高的疾病之一,其中,以急性冠状动脉综合征(ACS)病情最为凶险,而近70%的急性冠脉事件并不是由显著地冠状动脉狭窄引起,而是由冠状动脉易损斑块(vulnerable plaque)破裂造成的急性狭窄,以及其后血栓形成所致,因此冠状动脉易损斑块是导致急性冠状动脉综合征的主要元凶,因此需要早期发现易损斑块并积极进行干预。近两年来,CT、MRI、血管内超声(IVUS)和光学相干断层成像(OCT)广泛应用于易损斑块的评估并取得显著进展,而分子影像学能从分子层面揭示易损斑块形成机制以及更加早期识别斑块进行。本文简要总结近两年影像学方法对易损斑块的最新研究进展及热点。     

神经元编码选择性改变的研究

大脑皮层的神经元究竟怎样把不同的信息经过处理加工后使之相互联系起来 ,即如何发挥其信息整合功能 ,是神经科学的重要研究课题。例如 ,参与控制眼球运动方向的外侧顶内区 (ｌａｔｅｒａｌｉｎｔｒａｐａｒｉｅｔａｌａｒｅａ ,ＬＩＰ)神经元可编码空间位置信息 ,但并不编码颜色等与空间位置无关的视觉信息。若颜色信息与眼球运动方向相联系 ,中枢是否会将两种信息整合起来 ,即使ＬＩＰ参与颜色信息编码呢 ?Ｔｏｔｈ和Ａｓｓａｄ最近的一项研究回答了这个问题。他们将两组电极分别插入两只恒河猴的ＬＩＰ区 ,同时记录ＬＩＰ的神经元放电情…     

亚低温减少沙土鼠脑缺血后延迟性神经元死亡机制的研究

目的：研究亚低温对脑缺血后延迟性神经元死亡的影响及其与海马羟自由基产生以及纹状体多巴胺和ＡＴＰ含量变化的关系。方法：沙土鼠前脑缺血再灌注模型,缺血１０ｍｉｎ,应用病理检查方法判断海马ＣＡｌ锥体细胞死亡的数目。动物随机分为假手术组、缺血组、缺血再灌注组和亚低温缺血再灌注组。高效液相加电化学检测器方法测定海马羟自由基和纹状体多巴胺的含量,高效液相紫外检测器法测定纹状体ＡＴＰ含量。结果：亚低温条件下沙土     

电针对脑缺血神经元凋亡影响的形态学研究

为了探讨针刺治疗“脑卒中”的机制,本研究以大鼠一侧大脑中动脉栓塞后再灌注为动物模型,分别以ＴＵＮＥＬ法和ＰＩ染色法观察电针改善脑缺血性神经元凋亡的情况。结果显示：①局灶性脑缺血能诱导神经元凋亡：缺血侧凋亡神经元数目明显多于对照侧,差异非常显著;②电针能明显抑制神经元凋亡：电针治疗组缺血侧梗塞区凋亡神经元数目明显减少。本文表明电针能抑制脑缺血性神经元凋亡。     

神经元微管蛋白的研究进展

神经元特殊形态的形成及维持主要依赖于神经元细胞骨架中微管的装配,在此过程中,涉及到微管的组成及其动力学性质,而最终形成了稳定的微管结构,在神经元中,这一结构为沿着神经突运输物质提供了基础。本文将主要在神经元微管的结构与功能,神经元微管蛋白异构基因的表达及其翻译后加工形式等方面的研究进展加以综述。     

肠道病毒71型致神经元病变的机制研究进展

中枢神经系统感染是由病原体侵犯中枢神经系统引起的一类具有较高的发病率和死亡率的疾病。病毒是引起中枢神经系统感染的重要病原体之一,其中肠道病毒71型在继发神经系统症状的重症手足口病患儿中较为常见。EV71致神经元病变是其感染中枢神经系统的基础,阐明肠道病毒71型致神经元病变的机制,不仅可以促进基础病毒学研究,也能为抗病毒药物的开发提供思路,对临床肠道病毒71型致中枢神经系统感染的治疗提供支持。本文主要从肠道病毒71型侵入神经元的受体途径、损伤神经元的线粒体途径、诱导凋亡与自噬、感染胶质细胞后对神经元的旁观者效应、免疫病理机制以及病毒自身因素等多个方面,对肠道病毒71型致神经元病变机制展开综述。     

新的易损斑块血清标志物妊娠相关蛋白A研究进展

冠状动脉易损斑块破裂或腐蚀继发血栓形成是急性冠脉事件发生的病理基础,寻找易损斑块新血清标记物对于早期识别和干预高危患者至关重要。新近发现妊娠相关蛋白A(PAPP-A)参与动脉粥样硬化的发生发展,并且与斑块的不稳定性关系密切,是冠心病患者不良事件的预测因子。本综述主要介绍妊娠相关蛋白-A的生物学特性及其与心血管疾病以及易损斑块关系的研究进展,为临床诊断和治疗带来新的思路。     

Ceramide selectively inhibits apoptosis-associated events in NGF-deprived sympathetic neurons

Ceramide manifests both neurotoxic and neuroprotective properties depending on the experimental system. Ito and Horigome previously reported that ceramide delays apoptosis in a classic model of developmental programmed cell death, i.e. sympathetic neurons undergoing NGF deprivation.1 Here, we investigated the actions of ceramide upon the biochemical and genetic changes that occur in NGF deprived neurons. We correlate ceramide's neuroprotective actions with the ability of ceramide to antagonize NGF deprivation-induced oxidative stress and c-jun induction, both of which contribute to apoptosis in this model. However, ceramide did not block NGF deprivation-induced declines in RNA and protein synthesis, suggesting that ceramide does not slow all apoptosis-related events. Overall, these results are significant in that they show that ceramide acts early in the death cascade to antagonize two events necessary for NGF-deprivation induced neuronal apoptosis. Moreover, these results dissociate declines in neuronal function, i.e. macromolecular synthesis, from the neuronal death cascade.     

中国典型生态脆弱区生态化学计量学研究进展

在人类活动和自然环境变化的相互作用下,生态脆弱区生态系统随之变迁,荒漠化、盐碱化、水土流失、植被生产力下降等是生态脆弱区面临的重要问题。生态化学计量学作为当前多学科交叉研究的热点领域,强调从生态系统能量与元素平衡角度,揭示元素生物地球化学循环和生态系统对环境变化的调控机制。为了促进对生态脆弱区碳（C）、氮（N）、磷（P）生态化学计量的深入理解,本文重点总结了近年来有关我国典型生态脆弱区植物、凋落物、土壤和土壤微生物量C、N、P生态化学计量及其对环境变化响应的研究成果,并展望未来研究方向,以期促进生态化学计量学的发展和生态脆弱区生态保护与恢复研究。研究表明,植物-凋落物-土壤-土壤微生物系统C、N、P化学计量具有较强相关性,并受土壤因子、气候因子、生物因子和人类活动的显著影响。在生态脆弱区,我国北方荒漠及荒漠化地区由于较高的N∶P比值易受P限制,而青藏高原脆弱区、西南岩溶石漠化地区和黄土高原脆弱区等生态脆弱区更易受N限制;随着植被恢复,养分限制逐渐由N限制向P限制转变。生态脆弱区相对较低的养分含量和C∶N∶P比值或许可在一定程度上解释植被生产力较低的原因,而具有较高N、P化学计量内稳性的植物在贫瘠环境中具有较强竞争力和更高稳定性。今后可加强多尺度、不同生态系统植物-凋落物-土壤-土壤微生物系统生态化学计量和长期、多因子交互控制实验的研究。     

Charybdotoxin selectively blocks small Ca-activated K channels in Aplysia neurons

The action of charybdotoxin (ChTX), a peptide component isolated from the venom of the scorpion Leiurus quinquestriatus, was investigated on membrane currents of identified neurons from the marine mollusk, Aplysia californica. Macroscopic current recordings showed that the external application of ChTX blocks the Ca-activated K current in a dose- and voltage-dependent manner. The apparent dissociation constant is 30 nM at V = -30 mV and increases e-fold for a +50- to +70-mV change in membrane potential, which indicates that the toxin molecule is sensitive to approximately 35% of the transmembrane electric field. The toxin is bound to the receptor with a 1:1 stoichiometry and its effect is reversible after washout. The toxin also suppresses the membrane leakage conductance and a resting K conductance activated by internal Ca ions. The toxin has no significant effect on the inward Na or Ca currents, the transient K current, or the delayed rectifier K current. Records from Ca-activated K channels revealed a single channel conductance of 35 +/- 5 pS at V = 0 mV in asymmetrical K solution. The channel open probability increased with the internal Ca concentration and with membrane voltage. The K channels were blocked by submillimolar concentrations of tetraethylammonium ions and by nanomolar concentrations of ChTX, but were not blocked by 4-aminopyridine if applied externally on outside-out patches. From the effects of ChTX on K current and on bursting pacemaker activity, it is concluded that the termination of bursts is in part controlled by a Ca-activated K conductance.     

Rotenone selectively kills serotonergic neurons through a microtubule-dependent mechanism

As a major co-morbidity of Parkinson's disease (PD), depression is associated with the loss of serotonergic neurons. Our recent study has shown that midbrain dopaminergic neurons are particularly vulnerable to microtubule-depolymerizing agents including rotenone, an environmental toxin linked to PD. Here we show that rotenone also selectively killed serotonergic neurons in midbrain neuronal cultures. Its selective toxicity was significantly decreased by the microtubule-stabilizing drug taxol and mimicked by microtubule-depolymerizing agents such as colchicine and nocodazole. Microtubule depolymerization induced by rotenone or colchicine caused vesicle accumulation in the soma and killed serotonergic neurons through a mechanism dependent on serotonin metabolism in the cytosol. Blocking serotonin synthesis or degradation, as well as application of antioxidants, significantly reduced the selective toxicity of rotenone or colchicine. Inhibition of vesicular sequestration of serotonin exerted a selective toxicity on serotonergic neurons that was mitigated by blocking serotonin metabolism. Over-expression of parkin, a protein-ubiquitin E3 ligase that strongly binds to microtubules, greatly attenuated the selective toxicity of rotenone or colchicine. The protective effects of parkin were abrogated by its PD-linked mutations. Together, our results suggest that rotenone and parkin affect the survival of serotonergic neurons by impacting on microtubules in opposing manners.     

Ethanol selectively potentiates GABA-mediated inhibition of single feline cortical neurons

Ethanol (alcohol) released from micropipettes by electro-osmosis (up to 10 nA from 0.3 M in 165 mM NaCl solution) potentiated the inhibition of firing of single cortical neurons produced by iontophoretically-applied pulses of γ-aminobutyric acid (GABA), whereas it had no effect or a mild antagonistic effect on the inhibition produced by pulses of glycine, and had an antagonistic effect on the inhibition produced by pulses of serotonin or dopamine. The potentiation of iontophoretically-applied GABA was also obtained by intravenously-applied ethanol (0.2–2 mg/kg). Furthermore, ethanol applied by electro-osmosis or intravenously in the same doses potentiated the inhibition of firing of single cortical neurons evoked by electrical stimulation of the surface of the cerebral cortex, which is believed to be mediated by endogenous GABA. These findings may have implications for alcoholism, since GABAergic neurotransmission is involved in the mechanism of action of anxiolytic drugs and anxiety is involved in the etiology of alcoholism.     

L-六碳糖形成机制的研究进展

糖及其衍生物在许多初级或次级代谢过程中发挥着重要作用。糖结构与功能的多样性和糖在疾病诊断与治疗中的重要性推动了糖生物学的快速发展。D型糖,尤其是D-六碳糖在糖中占据着主导地位,L-六碳糖也是许多重要糖蛋白复合物、多糖及抗生素的组成成分。了解L-六碳糖的形成机制有助于理性改造糖的结构并开发其应用价值。L-六碳糖通常由3,5位差向异构酶或5位差向异构酶催化D-六碳糖的C5位异构化形成,这种转变赋予了糖在构型上的多样性,并在许多天然产物中起决定生物活性的作用。对3,5位差向异构酶和5位差向异构酶的功能及晶体结构的研究揭示了L-六碳糖的形成机制。本文综述了L-六碳糖形成过程中不同类型的3,5-位差向异构酶和5-位差向异构酶的催化机制,揭示L-六碳糖在生理和医药领域的重要意义。     

昆虫味觉感受机制研究进展

很多昆虫具有极其灵敏的味觉感受系统, 在其取食选择、 交配和产卵等过程中起重要作用。相对于昆虫的嗅觉机制, 对昆虫味觉感受机制的研究较少。传统的味觉感受研究主要集中在味觉感器外部形态、 味觉电生理和行为学上。近年来随着分子遗传学、 生物信息学和神经生物学技术的应用, 昆虫味觉的研究不断深入, 主要体现在下列两方面： （1）味觉受体方面, 通过分子生物信息学等手段获得了多种昆虫的味觉受体, 不同种昆虫之间受体数目差异较大, 不同受体之间氨基酸的相似性较低。通常, 根据味觉受体配体物质的性质可以把味觉受体分为取食抑制素受体和取食刺激素受体两大类。（2）味觉神经元的投射及味觉编码机制方面, 多个研究表明昆虫外围味觉神经元在中枢神经系统中的投射部位为咽下神经节和后脑, 但是不同性质的受体神经元投射的具体位置有所不同。本文对昆虫味觉感器和神经元的基本特征, 味觉受体的进化、 表达和功能, 味觉神经元在中枢神经系统中的投射, 味觉神经元的编码机制及味觉可塑性等进行了综述。