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    共找到 医药卫生相关的 580019篇文献

    S2A-4 Epigenetic Mechanisms Underlying Fetal AlcoholSpectrum Disorders 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: CHEN Shao-yu 阅读量: 980

    Maternal alcohol consumption is the leading known non-genetic cause ofmental retardation. Prenatal alcohol exposure can cause a range of structural and functional birthdefects,which are defined as Fetal Alcohol Spectrum Disorders (FASD)。 Growing evidencesuggests that excessive cell death in selected cell populations is a major component of thepathogenesis of FASD. This suggests that a strategy for protecting against ethanol’s teratogenesisby epigenetically regulating the genes involved in the apoptotic pathway is promising foreffective intervention and prevention of FASD. We have recently found that treatment withethanol resulted in a significant decrease in miR-125b expression in neural crest cells (NCCs)and mouse embryos. We also validated that Bcl-2 antagonist killer 1 (Bak1) and p53-upregulatedmodulator of apoptosis (PUMA) are the direct targets of miR-125b in NCCs. In addition 展开

    Epigenetic Mechanisms Underlying Fetal AlcoholSpectrum Disorders

    S2B-3 The Translocator Protein (18 kDa),A PotentialNovel Drug Target of Mental Disorders 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: LI Yun-feng 阅读量: 2300

    Background:Recently,the translocator protein( 18 kDa)( TSPO),previouslycalled peripheral benzodiazepine receptor (PBR),has received increased attention in thepathophysiology of several kinds of neuropsychiatric disorders. The aim of the present study wasto evaluate the exact role of TSPO in the pathophysiology and treatment of mental disorders.Methods:Firstly,by using TSPO WT/KO mice or the lentiviral vectors mediating TPSOoverexpression,we studied the important role of TSPO in the anxiolytic and antidepressanteffects. The results obtained in this studies provided new insights into the potential target ofTSPO for the treatment of mental disorders. Secondly,we determined the the target profile of YLIPA08,a potent and selective TSPO ligand synthesized by our institute. And we then measured itsanti-PTSD,antidepressant and anxiolytic-like effects in various mouse and rat models. Finally, 展开

    Translocator Protein (18 kDa) PotentialNovel Drug Target Mental Disorders

    S2B-5 Rapid Release of GABA Inhibiting Epilepsy inVivo 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: DING Ran 阅读量: 3906

    Objective:Epilepsy is a multi-etiological brain dysfunction syndromecharacterized by synchronously repeated spontaneous discharges from neuronal cells. Itspathogenesis involves excitatory / inhibitory imbalance,ion channel abnormalities and may berelated to the abnormal structure and function of neurotransmitter receptors. The research wasto observe the effects of rapid increase inhbitory neurotransmitter GABA on the excitatory /inhibitory imbalance,ion channel abnormalities and abnormal neurotransmitter receptors in livingepileptic mice from the level of free moving animal,cell,sub-cell and receptor. Methods: Thetechniques of fiber photometry and laser uncage of Rub-GABA for epileptic free moving miceinduced by administration of Kainic acid (KA) or 4-AP 展开

    Rapid Release GABA Inhibiting Epilepsy Vivo

    S3A-1 Impaired mRNA Translational Capacity isCorrelated with Aging-Dependent Memory Deficitsand Behavioral Inflexibility 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: YANG Wen-zhong 阅读量: 2518

    Objective:Understanding of the molecular mechanisms underlying age-associatedcognitive impairments will not only contribute to our general knowledge about “aging” biology,butalso provide insights for more effective strategies to prevent and improve the quality of life for bothnormal aging and pathological aging such as Alzheimer’s disease (AD)。 multiple lines of evidencesuggest that subtle morphological and/or biochemical neuronal changes,instead of profound loss ofneurons,is responsible for aging-related impairments of cognition and synaptic plasticity,which is oftenmeasured in vertebrates as long-term potentiation (LTP),a synaptic model for memory. A substantialbody of evidence demonstrates that de novo protein synthesis (mRNA translation) is indispensable tomaintain long-lasting forms of memory and synaptic plasticity. Of interest 展开

    aging memory synaptic plasticity LTP protein synthesis eEF2 mTOR Alzheimer’s disease

    S3A-2 The Effect of PHA-543613 on Memory Disordersin Presenilin1 and Presenilin2 Conditional DoubleKnockout Mice 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: WANG Jia-yue 阅读量: 1625

    The mutation in the amyloid-beta precursor protein (APP) and presenilin genes(PSEN1 and PSEN2) cause autosomal dominant Alzheimer’s diease( ADAD) which is typicallyassociated with early-onset familial Alzheimer’s disease (FAD),however,the mechanism bywhich presenilin mutations cause memory disorders and neurodegeneration remains poorlyunderstood. In the present study,using Presenilin-1 and Presenilin-2 double knockout mice(cDKO mice),we observed that the impaired spatial reference memory,spatial working memoryand contextual fear memory in cDKO mice. Consistently,deficits of basal synaptic transmissionand LTP formation,as well as down-regulation of PI3K/Akt signaling pathway at hippocampusin cDKO mice. Furthermore,we found the expression levels of α7-nicotinic ACh receptors(α7nAChRs),NMDAR and AMPAR composition subunits,which related to synaptic plasticityand memory,were decreased at hippocampus in cDKO mice. Importantly 展开

    Alzheimer’s disease presenilin neuronal apoptosis synaptic plasticity memory

    S3A-5 Advantageous Features and Novel Mechanisms ofChinese Herbal Medicine in Treating Depression andDementia 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: CHEN Gang 阅读量: 2028

    Background:Conventional medicine has pronounced disadvantage in delayedonset in treating depression,and there was no effective drugs on treating Alzheimer’s diseases.Chinese herbal medicine has been widely used for treatment these disorders,whereas the researchthat test the advantageous features of TCM treatment is lacking. Aims:I will present our studyon detection of the advantageous features of treatment of depression and dementia using herbalmedicine,and the novel mechanism underlying the effects,focusing on repair of neural plasticityassociated with depression or dementia. Results:In preclinical studies,a single dose of Yuejurapidly attenuates the depression-like symptoms in various animal models and the antidepressanteffects could last even longer than ketamine,the prototype fast-acting antidepressant. We alsorevealed the critical neuromolecular mechanisms involving improved neural plasticity by Yueju.Moreover 展开

    Advantageous Features Novel Mechanisms ofChinese Herbal Medicine Treating Depression Dementia

    S3B-2 D1 Receptor-Mediated Endogenous tPA UpregulationContributes to Acute Blood Brain Barrier Damage 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: WANG Xiao-na 阅读量: 874

    Background:Disruption of the blood brain barrier (BBB) integrity at the earlystage of ischemia is becoming a critical target to reduce hemorrhage transformation (HT) becauseof the potential to predict HT. However,the mechanism underlying early BBB damage is notvery clear. It was reported that after acute ischemia,there was a significant increase of dopaminerelease in striatum where we have reported BBB damage as well as upregulation of HIF-1α after2 h ischemia. Objective:In current study,we aimed to investigate the role of dopamine signal 展开

    cerebral ischemia endogenous tissue plasminogen activator dopaminereceptor blood brain barrier tight junction proteins

    基于Nampt 的脑卒中治疗策略 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: 缪朝玉 阅读量: 760

    我们希望通过瞄准机体内在防御机制,挖掘脑卒中治疗新靶标和新药物。烟酰胺磷酸核糖转移酶(Nampt)是NAD 合成限速酶,NAD 参与几百个氧化还原反应、生产ATP 能量以及引发SIRTs 等多种酶的信号转导,Nampt-NAD-SIRTs 轴是机体重要的防御系统。早就知道脑缺血NAD 耗竭导致脑细胞死亡,而研究Nampt 作为脑卒中治疗靶标以及基于该靶标的新药发现还是近十年的事,我们是这个领域早期研究者,拥有该领域相关专利多项,并发表一系列论文。当前抗脑卒中靶标Nampt 已得到全世界多家实验室验证,在此重点介绍基于Nampt 的抗脑卒中治疗策略研究:①Nampt 激活剂?;贜ampt 酶活性的高通量筛选,完成了5.5 万个小分子筛选,确认了结构多样的新型Nampt 抑制剂,发现了首个Nampt 荧光探针化合物,测试到一个潜在的Nampt 激活剂具有抗脑卒中活性。②Nampt 重组蛋白。离体细胞OGD 模型上,野生型Nampt 具有神经?;ぷ饔?,而突变失活型Nampt 则没有;脑室给Nampt可减轻脑缺血损伤;外周给Nampt 可通过血脑屏障发挥作用。③Nampt 表达提高。病毒介导的脑局部过表达Nampt、Nampt 过表达转基因小鼠、神经元特异性Nampt 过表达转基因小鼠,以及药物、缺血预适应等引起的Nampt 表达提高,均可发挥抗脑缺血损伤作用。④Nampt 直接酶产物烟酰胺单核苷酸(NMN)。NMN 抗脑缺血损伤具有量效关系,缩小脑梗死体积,改善神经功能缺陷;可促进脑缺血后神经再生,有利于脑功能康复;能减轻脑缺血tPA 治疗引起的出血转化不良反应;对脑出血损伤也有神经?;ぷ饔?。作用机制主要涉及NAD-SIRTs 通路,也有研究提示NMN 还可抑制PARP1 依赖的NAD 耗竭。⑤促进NMN 生成的烟酰胺核糖(NR)。NR 具有抗脑卒中作用。这些策略研究为发展基于Nampt 的脑卒中治疗手段奠定了基础。 展开

    Nampt 脑卒 治疗策略

    S6B-4 Roles of the Basal Ganglia in Sleep-WakeRegulation 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: HUANG Zhi-li 阅读量: 3582

    The basal ganglia (BG) act as a cohesive functional unit that regulates motorfunction,habit formation,and reward/addictive behaviors. However,it is still not well understoodhow the BG maintains wakefulness and suppresses sleep to achieve all these fundamentalfunctions until genetically engineered systems developed these years. We focused on theadenosine A2A and dopamine D1 Receptors (R) in the BG and obtained following 4 findings:① Nucleus accumbens (NAc) dopamine D1R-expressing neurons are essential in controllingwakefulness and are involved in physiological arousal via the lateral hypothalamus and midbraincircuits;② The rostromedial tegmental nucleus (RMTg),also called the GABAergic tail of theventral tegmental area 展开

    adeno-associated virus optogenetics DREADD basal ganglia sleep-wakeregulation

    NP-8 Moderate Brain Injury Causes NeurobehavioralDeficits and Effects of Aerobic Exercise 收藏

    期刊: 神经药理学报 刊期: 2018年第0期 作者: WANG Ji-hui 阅读量: 939

    Objective:Moderate traumatic brain injury (TBI) can lead to a lifetime ofphysical,cognitive,emotional,and behavioral changes. Moreover,the secondary brain injury(SBI) during subacute and chronic phase after TBI could be blamed for these deficits. Exerciseis widely recognized as promoting health and improving bad moods,but the mechanisms bywhich exercise affects SBI are still unclear. Methods:Lateral fluid percussion (LFP) methodwas used to fabricate moderate TBI in motor and somatosensory cortex of the C57 BL/6 Jmice. A 4-weeks voluntary running wheel exercise with 6-day training per week was modified 展开

    traumatic brain injury neurobehavior deficits electrophysiological changes aerobic exercise

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