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Objective To count the number of ribbon synapses in cochlear inner hair cell using three-dimensional reconstruction model.

目的利用三维建模的方法对耳蜗内毛细胞带状突触进行计数分析,解决由于内毛细胞带状突触数量少、位置深在造成的计数困难,为内毛细胞带状突触的可塑性研究提供有效可靠的计数方法。

The relative timing between the presynaptic and postsynaptic spiking determined the direction and the extent of synaptic changes.

在前突触与后突触的相对尖突激发时间,决定了神经突触改变的程度与方向。

Sperry showed that the regenerated retinal axons always innervated the original sites of termination in the optic tectum. This experiment strongly disprove the resonance hypotheses proposed by Paul Weiss, who suggested that the nerve growth and synapse formation are largely random events, and the precision of connections between nerve cells emerged by selectively eliminating the inappropriate connections, only at later developmental stage.

Sperry的实验在支持Cajal假说的基础上,进一步明确发育过程中轴突的生长及突触的形成具有内在决定性,并且有力地反驳了当时占主流地位的由Paul Weiss于1930~40年代提出的resonance hypothesis,后者认为轴突的生长和突触的形成大多是一些随机事件,成年脑中的精确联系是通过对随机形成的不恰当联系进行选择地消除形成的。

Using the intracellular recording technique for monitoring the excitatory postsynaptic potentials of CA1 pyramidal neuron and delivering an activator of protein kinase C and/or inhibitors of PKC and 〓/calmodulin-dependent protein kinase Ⅱ into postsynaptic cell in hippocampal slices, we studied the role of postsynaptic PKC and CaMKⅡ in long-term potentiation induced by high frequency stimulation at the CA1 synapses made by Schaffer collateral/commissural and perforant pathway afferents.

用电生理学方法在大鼠海马脑片CA1区锥体细胞记录Schaffer侧枝和穿通通路到CA1神经元突触的兴奋性突触后电位,通过送蛋白激酶抑制剂和激活剂进入突触后细胞,我们研究了突触后蛋白激酶C和依赖钙/钙调蛋白的Ⅱ型蛋白激酶在高频刺激诱导的长时程增强产生和维持中的作用。

Based on above results, we conclude that the synaptic depression of thalamic input to the cortex contributes to rapid adaptation in cortical neuron, and both the thalamocortical and intracortical synaptic transmission could then enhance the degree of adaptation.

基于以上结果,我们认为,持续刺激引起的丘脑—皮层突触的抑制对皮层神经元的快速适应有贡献,而丘脑—皮层突触以及皮层—皮层突触的放大机制都可以将这一特性进一步增强。

To clarify the effect of lidocaine oncholinergic synapse, we reconstructed a cultured soma–somachemical synapse model consisting of two identified visceraldorsal 4 (VD4) and left pedal e-1 (LPeD1) neurons from the snail, Lymnaea stagnalis , in vitro , and used it to determine how lidocaineaffects cholinergic synaptic transmission.

为了阐明利多卡因对胆碱能突触的影响,我们从椎实螺属 stagnalis 的蜗牛离体重建了含两种已被鉴定的内脏背4( VD4)和左足 e-1( LPeD1)神经元的培养体细胞-体细胞化学突触模型,来研究利多卡因如何影响胆碱能突触传递。

Two kinds changes of neuron plasticity are confirmed being related to GAP-43:(1)synaptic structural change makes GAP-43 increase ;(2) changes of synaptic transduction efficacy that long term potential and long term depression can alter GAP-43 phosphatize state and mRNA expression.

突触素(synaptophysin,P38)系一相对分子质量为38000的膜结构蛋白,存在于突触前囊泡膜,与突触的结构和功能密切相关。P38作为突触前终末特异性标记物,常用来反映突触的密度和分布。

Ltp and ltd at excitatory neuronal synapses are observed to be induced by precise timing of pre- and postsynaptic events.

兴奋神经元突触的ltp和ltd是由突触前和突触后活动的精确定时所诱导。

Thus, correlated pre-and postsynaptic activity alters not only the strength of the activated input, but also its dendritic integration with other inputs.

因此,突触前后神经元的相关活动不仅影响被激化突触的传递效率,还影响树突的信号整合特性。

Many lines of physiological and pharmacological evidence show that AMPA receptor desensitization plays an important role in fast excitatory synaptic transmission by affecting transmission efficacy of individual synaptic bouton, integrative functions of neuron, and synapse plasticity.

大量的生理学和药理学证据表明,AMPA受体失敏在快速兴奋性突触传递过程中起着重要的作用,对单个突触的传递效率、经元的整合功能和突触的可塑性均有影响。

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