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失眠症是常见的睡眠障碍之一,患者常伴有严重的主观认知功能障碍,但客观认知功能测试显示他们并不存在明显的认知功能损害。神经影像、神经生物化学和神经电生理学等方面的研究提示,失眠症患者可能存在潜在的认知功能损害的客观证据。本文对失眠症患者的认知功能损害特点进行阐述,并介绍在神经影像、神经生物化学和神经电生理学等方面潜在的认知功能损害的证据,分析其可能的原因。  相似文献   
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目的:探讨吗啡躯体依赖、精神依赖及戒断对雄性大鼠海马内神经甾体水平的影响。方法:腹腔注射递增剂量吗啡建立大鼠吗啡躯体依赖模型,纳洛酮诱发戒断症状;条件性位置偏爱实验建立吗啡精神依赖模型。高效液相色谱-质谱法测定大鼠海马和血浆中脱氢表雄酮(DHEA)及其硫酸酯(DHEAS)、孕烯醇酮(PREG)及其硫酸酯(PREGS)和别孕烯醇酮(AP)含量。结果:大鼠吗啡躯体依赖形成时海马内DHEA、PREG水平较对照组升高(0·88±0·19/0·67±0·17,t=2·52,P<0·05,10·94±2·02/7·53±2·64,t=3·24,P<0·01),血浆中DHEAS、PREGS水平较对照组升高(115·4±99·7/29·3±8·3,t=3·20,P<0·01;234·5±216·1/38·2±18·8,t=3·39,P<0·01);大鼠吗啡精神依赖形成时海马及血浆中DHEA水平降低(0·90±0·55,15·6±5·0/1·63±0·76,24·5±9·8,t=2·42,2·69,P<0·05),血浆中DHEAS水平显著升高(187·4±44·8/136·7±30·7,t=2·88,P<0·05)。与纳洛酮对照组比较,大鼠吗啡戒断时海马内DHEA、AP、DHEAS、PREGS水平升高(t=2·33~3·96,P<0·05),血浆中PREG、AP、DHEAS和PREGS水平升高(t=3·72~4·82,P<0·01)。结论:吗啡依赖、戒断可影响大鼠海马内某些神经甾体的水平,表明内源性神经甾体可能参与吗啡依赖的形成。  相似文献   
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抑郁症神经生化和神经电生理学研究进展   总被引:7,自引:0,他引:7  
抑郁症的发病机制复杂,神经生化学理论是迄今最为“肯定”、并被临床药理“充分利用”的,用以阐述抑郁症发病的神经生物学机制,抑郁症的发生不但与去甲肾上腺素(NE)、5-羟色胺(5-HT)水平相关;也可能与多巴胺(DA)、乙酰胆碱(Ach)、神经肽、γ-氨基丁酸(GABA)能系统等多种神经递质及受体的功能紊乱有关,还与内分泌系统和神经营养因子系统等方面的异常有关。同时,抑郁症的发生还可能与神经认知功能的缺损及神经电生理学的改变有关。  相似文献   
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乙醇对大鼠神经行为及相关酶的影响   总被引:2,自引:0,他引:2  
[目的 ]探讨乙醇对大鼠神经行为效应及脑组织中相关酶的影响。 [方法 ]体重 160g左右的雄性SD大鼠2 5只 ,随机分为三组 ,每组为 9、8、8只 ,分别以 0 % (对照组 )、2 5 64 % (低剂量组 )、5 1 2 8% (高剂量组 )乙醇溶液 (浓度以V/V表示 )按 1 0ml/10 0g体重一次性灌胃染毒。 3 0min后 ,进行自发活动、转棒实验和方位水迷宫测试。在染毒 1h后 ,断头处死 ,取血测血中乙醇浓度 (BAC) ,取脑组织测丙二醛 (MDA)、超氧化物歧化酶 (SOD)、巯基化合物 ( SH )和胆碱酯酶活性。 [结果 ]高剂量组自发活动中的行走次数显著高于低剂量组和对照组 ;转棒测试 ,高、低剂量组在棒上停留时间均显著低于对照组 (P <0 0 1) ;水迷宫试验学习次数 ,在染毒前对照组明显高于染毒组 ,而在染毒后各组间差异无统计学意义 ;且上述改变与BAC相关显著。高剂量组SOD活性显著低于低剂量组和对照组。丙二醛、巯基水平及胆碱酯酶活性各组间无明显差异。 [结论 ]乙醇可降低大鼠对新环境的适应性、肌肉运动协调能力下降和学习记忆能力的减退 ,并和脑组织中SOD活性呈一定相关  相似文献   
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Summary With the intention of compensating for the deficit of endogenous dopamine (DA) in the basal ganglia of Parkinsonian patients by substitution with agents which directly stimulate central DA receptors, synthetic DA agonists have been introduced almost 20 years ago for the symptomatic treatment of Parkinson's disease. The original expectation that DA agonists would be able to completely restore extrapyramidal motor function in Parkinsonian patients has turned out as too mechanistic and simplicative. However, undoubtedly DA agonists have improved therapeutic possibilities in Parkinson's disease. Thus, clinical evidence from controlled chronic studies in patients indicates that the therapeutic results following the early application of DA agonists in combination with L-DOPA on a long-term base are superior to the respective monotherapy. However, none of the DA agonists currently employed for antiparkinsonian treatment i.e. apomorphine and the ergoline derivatives bromocriptine, lisuride and pergolide, is optimal with respect to pharmacokinetic properties (poor oral bioavailability with considerable intra-and interindividual variation) or pharmacological profiles (low selectivity for DA receptors in case of the ergot agonists). The pathophysiology underlying Parkinson's disease which turned out more complex than initially expected might provide another explanation for the limited therapeutic potential of DA agonists. Therefore, apart from summarizing the pharmacokinetics, biotransformation, neuropharmacology and neurobiochemistry, of the DA agonists employed clinically, the present article also reviews physiological aspects of (a) central dopaminergic neurotransmission including the topographical distribution of DA receptor subtypes and their functional significance, (b) the intracellular signal processing in striatal output neurons and (c) the intraneuronal mechanisms which integrate the various neurotransmitter signals converging on the striatal output neuron to a demand-adjusted effector cell response via the cross-talk between the different second messenger systems. Based on these considerations, potential pharmacological approaches for the development of improved antiparkinsonian drugs are outlined. There is a therapeutic demand for more selective and better bioavailable DA agonists. In particular, selective D-1 receptor agonists are highly desirable to provide a more specific probe than SKF 38 393 for clarifying the current controversy on the disparate findings in nonprimate species and monkeys or Parkinsonian patients, respectively, regarding the functional significance of D-1 receptors for the antiparkinsonian action of DA agonists or L-DOPA. The therapeutic importance of D-2 receptor activation is generally accepted; whether DA agonists combining a balanced affinity to both D-1 and D-2 receptors within one molecule (to some extent a property of apomorphine) might be superior to subtype-specific DA agonists remains to be tested clinically. Beside selective DA agonists with markedly increased absolute oral bioavailability, the following alternative approaches for the symptomatic treatment of Parkinson's disease seem worth pursuing: (a) diminuition of excitatory amino acid (EAA)-mediated neurotransmission in the basal ganglia output nuclei, e.g. by EAA receptor antagonists, (b) pharmacological manipulation of the intracellular second messenger signals generated by DA, EAA's or acetylcholine in the striatal output neurons. Furthermore, preliminary experimental evidence indicates that, apart from symptomatic treatment, a preventive (neuroprotective) therapy of Parkinson's disease might be conceivable with EAA receptor antagonists.Dedicated to Nils-Erik Andén in memoriam  相似文献   
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目的检测由骨髓基质细胞诱导分化而成的神经元样细胞能否分泌氨基酸类神经生物活性物质成分,从而推断是否具有神经元的生化特征。方法无菌条件下抽取新西兰大白兔骨髓,梯度密度离心分离获取兔骨髓基质细胞(BMSCs),在神经干细胞培养基及细胞因子0.5 μg/ml维甲酸(RA)、20 ng/ml胶质源性神经营养因子(GDNF)于体外诱导分化为神经干细胞及神经元样细胞,采用免疫细胞化学方法进行鉴定,并应用高效液相色谱法(HPLC)检测其氨基酸类生物活性物质的含量。结果BMSCs培养10 d可见细胞大而圆,免疫细胞化学检测Nestin抗原阳性;培养20 d可见具有长突起的神经元样细胞形成,神经元特异烯醇化酶(NSE)免疫细胞化学检查阳性,高效液相检测骨髓源性神经元样细胞含有高浓度的天冬氨基酸(Asp)、谷氨酸(Glu)、甘氨酸(Gly)、丙氨酸(Ala)。方差分析显示:随着BMSC培养天数的增加,其所含的Asp、Glu浓度也渐增加,RA GDNF组所含Asp生物活性物质与其余各组比较有显著性差异(P<0.01)。结论兔BMSCs在体外条件下可以增殖分化,增殖细胞表达Nestin,分化的细胞则可表达NSE特异性抗原,并含有高浓度的兴奋性和抑制性氨基酸类神经递质成分;RA和GDNF作为BMSCs的诱导剂,在BMSCs向神经干细胞分化中起有重要的促进作用。  相似文献   
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