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Routtenberg agrees with the view that it is the synapse that is modified in response to learning-associated activity, a position first articulated by Nobelist Ramony Cajal a century ago.

Routtenberg也认同突触(是由诺贝尔奖得主Ramony Cajal在一个世纪前发现的)可以被学习相关性激活所改变。

This method of weight changing between nodal point s is very similar to the readjustment of the stimulus signals by synapsis of the brain

这种改变节点间连接权重的方法类似于大脑的突触对刺激信号进行调节的现象

The acetylcholine,γ-aminobutyric acid and nitric oxide are major neurotransmitters for olfaction synaptic transmission in MB.

乙酰胆碱、γ-氨基丁酸和一氧化氮等是蘑菇体嗅觉突触传递的主要神经递质。

Complete resolution of detrusor overactivity was observed in 44% of BTX-A patients at 4 weeks, though this dropped to 25% by 24 weeks.

重链结构BTX对运动神经末梢突触前膜的结合及内化有关;轻链结构与BTX抑制神经递质的释放有关。

However, a growing number of studies suggest that excessive extracellular glutamate and resultant overstimulation of its receptors cause excitotoxic roles and lead to neuronal damage in several pathological conditions such as cerebral ischemia. Normally, the excitatory postsynaptic roles of glutamate are terminated by the activities of high-affinity sodium dependent glutamate transporters that locate on neuroglial cells and neurons near the synaptic cleft, which are thought to play important roles in inactivating released glutamate and keep it below toxic levels in the extracellular space.

在生理状态下,突触间隙中谷氨酸的清除取决于邻近神经胶质细胞及神经元上高亲和力、钠依赖性谷氨酸载体的活动,通过该载体的再摄取机制保持细胞外谷氨酸浓度于正常范围,这在预防谷氨酸的神经毒中起着重要的作用。

Ultimately, vulnerable groups of neurons atrophy and die in a process that may involve excitotoxicity (overstimulation of neurotransmitter receptors on neuronal surface membranes), collapse of calcium homeostasis, inflammation, and depletion of energy and growth factors. A form of apolipoprotein E, apoE4, contributes to the abnormal accumulation of A and tau, but probably also damages mitochondria and the cellular cytoskeleton. A , tau, apoE and -synuclein interact with many other molecules and modulate diverse signalling cascades that regulate neuronal activity and survival.

最后,易感神经元会萎缩直至死亡,原因可能有兴奋性中毒(神经递质对神经元表面受体的过度刺激引起),钙稳态失衡,炎症反应,能量和生长因子的耗尽。apoE4的产生可导致A肽和tau蛋白的异常聚合,可能也损害线粒体和细胞骨架。A肽、tau蛋白、apoE和突触核蛋白可与很多分子反应,也可调节不同信号级联反应,这些级联反应对于维持神经元活动性和生存性意义重大。

Changes in false operation group, rehabilitation group and the intracerebral synaptic structure parameter of the model group.

为此本实验采用右侧大脑中动脉缺血大鼠模型应用滚笼网状训练、平衡训练以及Morris水密宫训练后,观察假手术组、经康复训练的康复组和未经训练的模型组大鼠在Y-迷宫分辨学习能力和一次性被动回避反应记忆保持能力的行为模式以及海马CA3区突触结构参数测定、在体LTP记录和NMDA受体通道电流记录等方法研究康复训练对梗死大鼠学习记忆的影响及其机制。研究内容包括: 1。

Objective To investigate the expression and pathological function of postsynaptic density-93 (PSD-93) after rat focal ischemic middle cerebral artery occlusion/reperfusion.

目的:观察突触后密度-93基因在大鼠局灶性脑缺血再灌注皮质表达的变化,探讨其在缺血再灌注损伤中的病理作用。

These results do not support the hypothesis that excitatoryeffects of pentobarbital may alter synaptic plasticity.

这些结果不支持巴比妥的兴奋性作用能改突触可塑性的假说。

Objective: To observe the effects of functional electrical stimulation on motor function and expression of synaptophysin in penumbra field and contralesional field of rats with acute cerebral infarction.

目的:观察功能性电刺激对急性脑梗死大鼠运动功能和缺血半影区与镜区突触素表达的影响。

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