突触可塑性

突触可塑性相关物质及其在脑缺血后的变化

The Related Substance of Synaptic Plasticity and its Change after Cerebral Ischemia

不同针刺量对大鼠脑缺血后突触可塑性的影响

Effect of Acupuncture at Different Doses on Synaptic Plasticity of Rats After Cerebral Ischemia

鲫鱼视网膜水平细胞的Ca～（2+）动力学和突触可塑性

Ca ~( 2 + ) Dynamics and Synaptic Plasticity in Carp Retinal Horizontal Cells

颞叶癫痫大鼠海马CA1区突触可塑性与空间记忆能力关系的研究

The relationship between the synaptic plasticity in CA_1 region in hippocampus and the space memory ability in temporal lobe epileptic male rats

发育期补充DHA对大鼠海马突触可塑性的影响

The effects of supplemented with DHA on synaptic plasticity during development period in rats

慢性铝暴露对大鼠海马突触可塑性LTP影响及其机制研究

Effects and Mechanism of Chronic Exposure of Aluminum on Rats Hippocampus Synapse Plastic LTP

大量研究表明，NMDA受体参与了突触可塑性过程。

A mass of research indicate that NMDA receptor have been involved in the process of synaptic plasticity .

神经营养因子尤其是目前研究最多的BDNF对神经元的生长、分化、存活及突触可塑性方面具有非常重要的作用。

Neurotrophins especially the most studied BDNF are important for neuronal growth , differentiation , survival and synaptic plasticity .

结论：发育期锌缺乏不但可造成学习能力下降、海马突触可塑性受损，同时还可使脑组织中MT蛋白及其mRNA表达降低；

Conclusion : Zinc deficiency results not only in injury of learning ability and decrease of hippocampal synaptic plasticity , but also inhibition of MT and mRNA expression .

PKA信号通路在脑缺血后突触可塑性中的作用及针刺干预研究

The Mechanism of PKA Signaling Pathway in Synaptic Plasticity after Cerebral Ischemia and Intervention Studies of Acupuncture

实验结果如下：（1）MC可以在一定程度上修复铝中毒引起的突触可塑性损伤。

The results are as follows : ( 1 ) MC can , to some extent , repair the synaptic plasticity deficiency induced by aluminum exposure .

EGCG对铅致大鼠海马神经元突触可塑性和氧化损伤的修复作用及机制

The Reparation and Mechanism of EGCG on the Lead-induced Impairments of Oxidative Stress and Synaptic Plasticity in Rat Hippocampus

Morris水迷宫实验可以测试突触可塑性的行为学表现，其结果也表明经慢性阿片处理后，大鼠产生了相应的学习能力的缺陷。

Morris water maze test , which measures behavioral consequences of synaptic plasticity , showed parallel learning deficits after chronic exposure to opiates .

碘缺乏及甲状腺功能减退子代大鼠海马长时突触可塑性与PKC活性及GAP-43表达的实验研究

Experimental Study of Long-term Synaptic Plasticity and PKC Activity and GAP-43 Expression in the Hippocampus of Iodine Deficient and Hypothyroid Pup Rats

研究表明NF-KB与突触可塑性的信号转导有关，参与神经元可塑性的形成。

Studies show that NF & κ B is related to signal transduction of synaptic plasticity and neuron plasticity forming .

上调基因多为促炎症、应激反应相关基因；而下调基因则多为突触可塑性、囊泡运输、线粒体功能、蛋白质和DNA修复、神经激素等相关基因。

Most of the up-regulated genes are related to inflammations and stress responses , but large part of the down-regulated genes play roles in synapse plasticity , vesicular transportation , mitochondria function , protein and DNA repair , and neurohormone secreting .

突触可塑性被认为是学习记忆的神经生物学基础，长时程增强（long&termpotentiation，LTP）是突触可塑性的一种重要形式。

Long & term potentiation ( LTP ), an important form of synaptic plasticity , is believed to underlie learning and memory .

联合应用病毒表达载体系统，荧光成像技术和电生理技术研究泛素蛋白酶体系统（UPS）介导的蛋白降解在活性依赖性的突触可塑性中的作用。

To address the role of ubiquitin-proteasome mediated protein degradation ( UPS ) in activity-dependent synaptic plasticity a combination of a viral expression system , fluorescent imaging and electrophysiology will be employed .

不同刺激对条件性恐惧大鼠行为及海马CA1区突触可塑性的影响

Effects of different stimuli on behavior and synaptic plasticity in hippocampal CA 1 area of fear conditioned rats

长时程增强（LTP）和长时程抑制（LTD），作为突触可塑性变化的两种主要形式，被认为是学习记忆的可能机制。

Long-term potentiation ( LTP ) and long-term depression ( LTD ), two forms of synaptic plasticity , are believed to underlie the mechanism of learning and memory .

脑源性神经营养因子（Brain-DerivedNeurotrophicFactor，BDNF）表达受PACAP调节，在促进神经元存活、分化及突触可塑性方面起重要作用。

Brain-derived neurotrophic factor ( BDNF ) expression is increased by PACAP in neurons , and plays an important role in neuronal survival , differentiation and synaptic plasticity .

基因芯片检测耐PHT点燃鼠脑突触可塑性基因的表达

Detection of the differential expression of genes with synapse plasticity in brains of the PHT-resistant / non-resistant epileptic rats with cDNA microarray

海马突触可塑性，主要是指活动或经验依赖的长时程增强（Long-termpotentiation，LTP）和长时程抑制（Long-termdepression，LTD），被认为是海马依赖的学习与记忆的细胞分子基础。

Hippocampal activity-dependent or experience-dependent synaptic plasticity , including Long-term potentiation ( LTP ) and Long-term depression ( LTD ), is believed to be the cellular and molecular mechanism which underlies hippocampus-dependent learning and memory .

受PFOS潜在影响的神经功能和生物过程包括，中枢神经系统发育、神经发生、长时程增强或抑制（LTP/LTD）、学习与记忆、神经递质传递和突触可塑性等（P0.05）。

Significantly affected genes ( P0.05 ) were involved in central nervous system development , neurogenesis , long-term potentiation / depression , learning and memory , neurotransmission and synaptic plasticity .

CREB是神经元内多条信息传递途径的汇聚点，参与长时记忆形成和突触可塑性。

Multiple signal transduction pathways converge on CREB , which plays an essential role in the formation of long-term memory and synaptic plasticity .

脑源性神经生长因子（brain-DerivedNeurotrophicFactor，BDNF）是一种重要的神经营养因子。调节成年脑组织突触可塑性及促进树突和轴突的生长等是其主要作用。

Brain-derived neurotrophic factor ( BDNF ) is an important neurotrophin which has pleiotropic effects on modulating activity-dependent forms of synaptic plasticity , neuronal survival , neuronal development , dendritic arborization and axon growth .

海马诱发电位长时程增强现象（Long-termpotentiation，LTP），常被用来研究与突触可塑性密切相关的学习与记忆过程的分子机制。

Long-term potentiation ( LTP ) of hippocampal synaptic activity is the most popular and widely used model of synaptic plastic changes , which is considered to be related to learning and memory .

研究人员指出，酒精并不是通过杀死神经元细胞导致失忆发生的。实际上，是这些产生的甾体物质影响了突触可塑性，造成了LTP和记忆形成方面的损害。

The scientists point out that alcohol isn 't causing blackouts by killing neurons . Instead , the steroids interfere with synaptic plasticity to impair LTP and memory formation .

结论酸性寡糖971改善AD模型小鼠学习记忆功能可能与DNA损伤修复、神经生长、突触可塑性、免疫应答等相关基因的表达变化有一定关系。

Conclusion The protective effect of 971 on learning and memory ability of β - AP_ ( 25-35 ) - treated mouse may be related to the expression changes of genes involved in cell cycle , DNA repair , nerve growth , synaptic plasticity and immune response , etc.

NMDA受体广泛表达于中枢神经系统，介导突触可塑性的形成，调控神经元的基因表达，参与发育过程中神经网络的形成。

NMDA receptors are abundantly expressed in central nervous system . It mediates the induction of synaptic plasticity , modulates gene expression , and participates in the induction of neuronal networks during various developmental stages .