6种乳酸菌降解胆固醇的体外试验

分析了6种安全的乳酸菌菌种在不同条件下接种于体外高胆固醇的MRS-CHOL培养基中降解胆固醇的情况,以及培养液的pH值与胆固醇降解率的关系。结果表明,所用的6个菌种均可有效降解胆固醇,依次为Lp菌（28．088％）、3群菌（25．059％）、4群菌（24．922％）、Lf菌（24．554％）、Ld菌（22．248％）和5#菌（18．513％）,降解率随接种量的增加和培养时间的延长而增加,除Lf菌外,其它菌株都随胆固醇浓度的变化而出现先升后降的趋势,培养液的pH值与胆固醇的降解率呈负相关性,且都不显著。     

PICK1蛋白中BAR结构域的功能受其下游C末端酸性区域的调节

0 引言 人们普遍认为学习和记忆包含了突触效能的长时程变化,这种效能变化体现在长时程增强(LTP)和长时程抑制(LTD)两种现象[1].     

急性应激对小鼠空间学习记忆功能及海马和前脑皮层c-Fos蛋白表达的影响

采用足底电击急性应激模型,通过旷场实验和Morris水迷宫实验分别测试小鼠的行为和空间学习记忆能力;以免疫组织化学方法检测c—Fos蛋白在海马和前脑皮层的表达．结果显示,与对照组小鼠比较,急性应激组小鼠在新异环境下的自发行为明显降低（P〈0．05,P〈0．01）,而在水迷宫实验中,急性应激组小鼠空间学习记忆能力明显提高（P〈0．05,P〈0．01）;与对照组小鼠比较,急性应激组小鼠海马CA1区、齿状回和前脑皮层c—Fos蛋白的表达在应激后1h明显增强（P〈0．05,P〈0．05,P〈0．01）．结果提示,急性应激所致小鼠空间学习记忆功能的改变可能与c—Fos蛋白表达的上调有关．     

摄食水平对褐牙鲆幼鱼能量收支的影响

褐牙鲆幼鱼（体重0.71-4.16g;体长4.45-8.14cm)在24℃下保持5个摄食水平（0－最大）。投喂人工配合饲料饵料。褐牙鲆和干物质的吸收效率随摄食水平的增加而增加,平均为97.38%和76．73％。褐牙鲆排粪能（F）占摄食能的比例为0．95％－2．83％,随摄食水平的增加而减少;氮排泄（U）占摄食能比例为5．52％－6．77％,各摄食水平下变化不大;标准代谢耗能（Rs)占摄食能比例为1．05％－7．82％,随摄食水平的增加而减少;在各摄食水平条件下,摄食代谢耗能（Rf)占摄食能比例变化不大,平均为45．72％;生长能（G）占摄食能比例为32．67％－49．21％。随摄食水平增加而增加。在最大摄食水平时,褐牙鲆能量分配形式为：100C＝0．95F＋5．52U＋44．31R＋49．21G。     

东山湾叫姑鱼食性研究

本文分析了东山湾叫姑鱼的摄食习性、食料生物组成和摄食强度的季节变化。结果表明：东山湾叫姑鱼系广食性底层鱼类，以底栖生物食性为主，兼食游泳动物。长尾类、短尾类、鱼类和多毛类是叫姑鱼食料中的优势类群。食料生物组成随季节而变化。摄食率秋季最高（７４．１％）、春季最低（３９．８％）；胃饱满系数夏季最高（１１．２‰）、春季最低（７．５‰）。其生殖活动对摄食行为没有影响。     

PHPA/SDBS/Mg-Al-HTlc/H2O悬浮体流变性研究

研究了部分水解聚丙烯酰胺（PHPA）／十二烷基苯磺酸钠（SDBS）／Mg-Al类水滑石（Mg-Al-HTlc）／水悬浮体的黏度行为，分别考察了SDBS质量分数Ⅲ（SDBS）、HTlc质量分数w（HTlc）、w（SDBS）／w（HTlc）比及pH对体系黏度（田）的影响．发现在所研究的质量分数范围内，PHPA／SDBS体系的η随w（SDBS）的增大而下降；PHPA／SDBS／Mg-Al-HTlc悬浮体的η随w（HTlc）的增大先上升，后下降，在w（SDBS）／w（HTlc）=0．25附近出现一个最大值；随pH的增大，PHPA／SDBS／Mg-Al-HTlc悬浮体的η先上升，在pH为7．0～10．5之间出现一个平台，后下降．     

Hg(Ⅱ)在泉州湾滩涂沉积物上的吸附

研究了Hg（Ⅱ）在泉州湾滩涂沉积物上的吸附行为，并在此基础上初步探讨了其吸附机理．主要讨论了pH和温度对吸附作用的影响，并绘制了吸附等温线．实验结果表明，常温下Hg（Ⅱ）在泉州湾滩涂沉积物上的吸附平衡时间约需3h，吸附作用随pH的升高而增强，受温度的影响变化不大．其吸附行为既符合Freundlich型吸附等温式，又符合Langumuir型吸附等温式，说明其吸附机理非常复杂．     

巴基斯坦地震前热红外辐射增强现象

2005年10月8日,北京时间11时50分36秒,巴基斯坦发生7．8级地震（73．6°E,34．4°N）．文中分析了3个以震中为中心的互相嵌套的（半）椭圆环的热红外辐射随时间变化，发现震前震中区附近热红外辐射出现增强现象，上升趋势随着离震中的距离增大而减小，远离震中区270km后，已看不到上升趋势．另外，发震断层MFT也出现热辐射增强现象，非发震断层亮温上升趋势不明显．分析证实各研究区地表温度年变及太阳辐射输入的能量从9月份到10月份是逐渐下降的, 说明震中区热红外辐射增强现象可能与Pakistan 地震有关．     

Cu^2＋对金鱼摄食行为的抑制

研究四种不同浓度Ｃｕ２＋对金鱼摄食行为、学习和记忆能力的影响，及摘除嗅囊后摄食行为的改变，探讨其中毒的机理．实验结果：１）不同浓度Ｃｕ２＋液对金鱼摄食行为呈抑制效应，抑制的程度随Ｃｕ２＋浓度的增加而加深，表现为首次撞击食球的时间（下简称首次撞击时间）随着中毒的加深而推迟，摄食的频率亦随之降低．反映了中毒鱼学习记忆的能力都随着Ｃｕ２＋浓度的增加而减弱；２）中毒鱼体重增长率随Ｃｕ２＋浓度的增加而减少，甚至呈现负增长现象；３）摘除嗅囊鱼的摄食频率仅为正常的１／２，学习和记忆的能力也较差     

益母草(Leonurus artemisia)灭螺的机理研究

用益母草中水苏碱处理钉螺导致其酯酶同工酶（EST）、糖原（Gn）及总蛋白（TPr）变化的实验结果表明：处理1～2d后钉螺的酶活高于清水对照组，处理3～4d后钉螺的酶活最强，而处理5d后钉螺样品的酶活则大大减弱．在处理过程中，有时出现新的酶带，有时又有酶带消失．经低浓度水苏碱（小于0．60g／L）处理后钉螺软体的糖原含量上升，增加幅度从9．152％到58.72％，促进了钉螺的能量代谢；而在高浓度Ck于0．80g／L）处理后的钉螺软体的糖原含量下降，减少幅度从11．68％到76.16％，表明高浓度水苏碱处理液通过影响钉螺的能量代谢从而抑制其生长．水苏碱处理后蛋白质的减少幅度较小（从5．66％到13．69％），水苏碱处理液浓度变化与作用后蛋白质的减少似乎没有关系．     

分辨学习中海马CA1区不同传入通路的突触传递效能变化

采用电生理学与行为学的结合方法,通过慢性埋植微电极技术,观察到大鼠在明暗分辨学习的建立过程中,海马ＣＡ１区不同传入突触上（Ｓｃｈａｆｆｅｒ－ＣＡ１与Ｐｅｒｆｏｒａｎｔ Ｐａｔｈ－ＣＡ１）均同步产生传递效能的长时程增强（ＬＴＰ）变化,在产生这一习得性ＬＴＰ的幅度上,ＰＰ－ＣＡ１大于Ｓｃｈ－ＣＡ１,而对照的假性训练动物却均未见到有这种变化,差异显著（Ｐ〈０．０１）。结果表明ＣＡ１区的不同传入通路在参与     

Synaptic excitation produces a long-lasting rebound potentiation of inhibitory synaptic signals in cerebellar Purkinje cells.

Persistent changes in synaptic efficacy are thought to underlie the formation of learning and memory in the brain. High-frequency activation of an afferent excitatory fibre system can induce long-term potentiation, and conjunctive activation of two distinct excitatory synaptic inputs to the cerebellar Purkinje cells can lead to long-term depression of the synaptic activity of one of the inputs. Here we report a new form of neural plasticity in which activation of an excitatory synaptic input can induce a potentiation of inhibitory synaptic signals to the same cell. In cerebellar Purkinje cells stimulation of the excitatory climbing fibre synapses is followed by a long-lasting (up to 75 min) potentiation of gamma-aminobutyric acid A (GABAA) receptor-mediated inhibitory postsynaptic currents (i.p.s.cs), a phenomenon that we term rebound potentiation. Using whole-cell patch-clamp recordings in combination with fluorometric video imaging of intracellular calcium ion concentration, we find that a climbing fibre-induced transient increase in postsynaptic calcium concentration triggers the induction of rebound potentiation. Because the response of Purkinje cells to bath-applied exogenous GABA is also potentiated after climbing fibre-stimulation with a time course similar to that of the rebound potentiation of i.p.s.cs, we conclude that the potentiation is caused by a calcium-dependent upregulation of postsynaptic GABAA receptor function. We propose that rebound potentiation is a mechanism by which in vivo block of climbing fibre activity induces an increase in excitability in Purkinje cells. Moreover, rebound potentiation of i.p.s.cs is a cellular mechanism which, in addition to the long-term depression of parallel fibre synaptic activity, may have an important role for motor learning in the cerebellum.     

海马MF-CA3突触习得性LTP诱导后PPF效应的变化

采用电生理学与行为学结合的方法，通过慢性微电极埋植技术及双脉冲检测技术，观察大鼠海马MF-CA3突触在明暗辨别学习过程中形成习得性长时程增强（Long-term potentiation, LTP）后双脉冲易化（Paired-pulse facilitation, PPF）效应的变化. 结果表明:Mossy fibers-CA3（MF-CA3）突触习得性LTP形成前的PPF易化率为138.36%9.25%，形成后则为114.75%8.42%，差异极显著（p 0.01），而基线对照组在长达7天的检测中，PPF易化率稳定在140%左右. 研究结果显示，MF-CA3突触的习得性LTP的表达可能与突触前递质释放的改变有关.     

NMDA receptors in the visual cortex of young kittens are more effective than those of adult cats

Acidic amino acids, such as glutamate and aspartate, are thought to be excitatory transmitters in the cerebral neocortex and hippocampus. Receptors for these amino acids can be classified into at least three types on the basis of their agonists. Quisqualate-preferring receptors and kainate-preferring receptors are implicated in the mediation of synaptic transmission in many regions including the hippocampus and visual cortex, whereas N-methyl-D-aspartate (NMDA)-preferring receptors are thought to be involved in modulating synaptic efficacy, for example in longterm potentiation, a form of synaptic plasticity in the hippocampus. In the visual cortex of the cat and monkey, it is well established that synaptic plasticity, estimated by susceptibility of binocular responsiveness of cortical neurons to monocular visual deprivation, disappears after the 'critical' period of postnatal development. Here we report that during the critical period in young kittens, a selective NMDA-receptor antagonist blocks visual responses of cortical neurons much more effectively than it does in the adult cat. This suggests that NMDA receptors may be involved in establishing synaptic plasticity in the kitten visual cortex.     

Postsynaptic hyperpolarization during conditioning reversibly blocks induction of long-term potentiation

Activity-induced changes in the efficacy of synaptic transmission between neurones are central to several prominent theories of learning. In both in vivo and in vitro preparations of the hippocampus, a conditioning high-frequency stimulus delivered to afferent fibres results in a long-term potentiation of synaptic transmission at those inputs. Evidence has been provided supporting both presynaptic and postsynaptic sites as loci where critical events occur in the development of potentiation. In this study we report that long-term potentiation is reversibly blocked by intracellular injection of hyperpolarizing current in the postsynaptic cell during the conditioning high-frequency stimulus, suggesting the involvement of a voltage-dependent postsynaptic mechanism.     

Dendritic spine changes associated with hippocampal long-term synaptic plasticity.

Long-term enhancement of synaptic efficacy in the hippocampus is an important model for studying the cellular mechanisms of neuronal plasticity, circuit reorganization, and even learning and memory. Although these long-lasting functional changes are easy to induce, it has been very difficult to demonstrate that they are accompanied or even caused by morphological changes on the subcellular level. Here we combined a local superfusion technique with two-photon imaging, which allowed us to scrutinize specific regions of the postsynaptic dendrite where we knew that the synaptic changes had to occur. We show that after induction of long-lasting (but not short-lasting) functional enhancement of synapses in area CA1, new spines appear on the postsynaptic dendrite, whereas in control regions on the same dendrite or in slices where long-term potentiation was blocked, no significant spine growth occurred.     

Genetic enhancement of learning and memory in mice.

Hebb's rule (1949) states that learning and memory are based on modifications of synaptic strength among neurons that are simultaneously active. This implies that enhanced synaptic coincidence detection would lead to better learning and memory. If the NMDA (N-methyl-D-aspartate) receptor, a synaptic coincidence detector, acts as a graded switch for memory formation, enhanced signal detection by NMDA receptors should enhance learning and memory. Here we show that overexpression of NMDA receptor 2B (NR2B) in the forebrains of transgenic mice leads to enhanced activation of NMDA receptors, facilitating synaptic potentiation in response to stimulation at 10-100 Hz. These mice exhibit superior ability in learning and memory in various behavioural tasks, showing that NR2B is critical in gating the age-dependent threshold for plasticity and memory formation. NMDA-receptor-dependent modifications of synaptic efficacy, therefore, represent a unifying mechanism for associative learning and memory. Our results suggest that genetic enhancement of mental and cognitive attributes such as intelligence and memory in mammals is feasible.     

Context-enabled learning in the human visual system

Training was found to improve the performance of humans on a variety of visual perceptual tasks. However, the ability to detect small changes in the contrast of simple visual stimuli could not be improved by repetition. Here we show that the performance of this basic task could be modified after the discrimination of the stimulus contrast was practised in the presence of similar laterally placed stimuli, suggesting a change in the local neuronal circuit involved in the task. On the basis of a combination of hebbian and anti-hebbian synaptic learning rules compatible with our results, we propose a mechanism of plasticity in the visual cortex that is enabled by a change in the context.     

Structural basis of long-term potentiation in single dendritic spines

Dendritic spines of pyramidal neurons in the cerebral cortex undergo activity-dependent structural remodelling that has been proposed to be a cellular basis of learning and memory. How structural remodelling supports synaptic plasticity, such as long-term potentiation, and whether such plasticity is input-specific at the level of the individual spine has remained unknown. We investigated the structural basis of long-term potentiation using two-photon photolysis of caged glutamate at single spines of hippocampal CA1 pyramidal neurons. Here we show that repetitive quantum-like photorelease (uncaging) of glutamate induces a rapid and selective enlargement of stimulated spines that is transient in large mushroom spines but persistent in small spines. Spine enlargement is associated with an increase in AMPA-receptor-mediated currents at the stimulated synapse and is dependent on NMDA receptors, calmodulin and actin polymerization. Long-lasting spine enlargement also requires Ca2+/calmodulin-dependent protein kinase II. Our results thus indicate that spines individually follow Hebb's postulate for learning. They further suggest that small spines are preferential sites for long-term potentiation induction, whereas large spines might represent physical traces of long-term memory.     

Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons

How do drugs of abuse modify neural circuitry and thereby lead to addictive behaviour? As for many forms of experience-dependent plasticity, modifications in glutamatergic synaptic transmission have been suggested to be particularly important. Evidence of such changes in response to in vivo administration of drugs of abuse is lacking, however. Here we show that a single in vivo exposure to cocaine induces long-term potentiation of AMPA (alpha-amino-3-hydroxy-5-methyl-isoxazole propionic acid)-receptor-mediated currents at excitatory synapses onto dopamine cells in the ventral tegmental area. Potentiation is still observed 5 but not 10 days after cocaine exposure and is blocked when an NMDA (N-methyl-d-aspartate) receptor antagonist is administered with cocaine. Furthermore, long-term potentiation at these synapses is occluded and long-term depression is enhanced by in vivo cocaine exposure. These results show that a prominent form of synaptic plasticity can be elicited by a single in vivo exposure to cocaine and therefore may be involved in the early stages of the development of drug addiction.