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By using freshly isolated SD rat cerebrocortical synaptosomes and KC1 as chemical stimulant to depolarize, we studied the effects of etomidate on KCl-induced increased intrasynaptosomal calcium concentrations, voltage-gated calcium channel subtypes on presynaptic membrane and neurotransmitters release from synaptosomes respectively, via neurochemical and inverse phase high performance liquid chromatographic methods.

我们利用SD大鼠新鲜分离的大脑皮层突触体作为研究对象,以KCl作为化学刺激剂去极化,采用神经化学方法(Fura-2作为钙离子指示剂)和高效液相测定法,分别就依托咪酯对去极化诱发突触体内钙离子浓度升高的影响,突触体膜上电压门控性钙通道亚型的作用以及由此引起的对神经递质释放的影响进行了实验研究。

The table of contents include 15 parts, early events in neural development; neuronal differentiation; pattern and positional information; movement and migration of neurons; axon outgrowth and the generation of stereotyped nerve patterns; neuronal death during development; trophic effects of targets on neurons; long-term effects of neurons on their targets; formation of synapses; selective synaptic connections; the molecular basis of neuronal recognition; rearrangement of developing neuronal connections; maintenance and modifiability of synapses; the development of behavior; principles of neural development.

内容包括15部分,早期神经发育事件;神经细胞分化;模式与位置信息;神经元运动及迁移;轴突生长与固定的神经模式的形成;发育过程中的神经细胞死亡;对神经细胞靶向的营养效应;神经细胞对它们靶向的长期效应;突触形成;选择突触连结;神经细胞识别的分子基础;发育过程中神经细胞连结的重置;突触保持和改变;行为发育;神经发育原理。

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。

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。

Synaptic inputs activated repetitively within 20 ms before spiking of the tectal neuron become potentiated, whereas subthreshold inputs activated within 20 ms after spiking become depressed.

在四叠体突触尖波20ms前连续被激发的突触输入将造成突触电位化,然而在尖波产生的20ms后的小于临界输入将造成突触抑制。

We tested whether inhibitory GABAergic synaptic transmission regulates Xenopus optic tectal cell dendritic arbor development in vivo by expressing a peptide corresponding to an intracellular loop ofthe gamma2 subunit of type A GABA receptors GABA(AR, which is required to anchor GABA receptors to the postsynaptic scaffold.

我们想证明如下设想:抑制性GABA能突触传递是否能调节早蟾视顶盖细胞的树突发育。因为GABA受体的gamma2亚基有一段细胞内的跨膜端序列,这段序列对锚定GABAA受体到突触后膜是必须的,所以我们的主要方法是设计了一段特异性的争对细胞内段的序列,这样就特异性的阻断了单个细胞GABA能的突触传递。

Synaptic inputs activated repetitively within 20 ms before spiking of the tectal neuron become potentiated, whereas subthreshold inputs activated within 20 ms after spiking become depressed.

在四叠体突触尖波20ms前连续被激发的突触输入将造成突触电位化,然而在尖波产生的20ms后的小於临界输入将造成突触抑制。

Using electron microscopy, the SPR-LI products in DCN neurons were seen not only in postsynaptic sites, but also in non-synaptic regions of the perikarya and dendritic profiles.

在电镜下证明SPR免疫阳性产物不仅位于突触后部位而且分布于胞体和树突的非突触部位,有42%的SPR阳性树突与SP阳性终末形成突触连结。

The quantity of the synapses in neuropil of the model group decreasedsignificantly(P<0.01), and the typical synapse structure was destroyed; the quantity of thesynapses in neuropil of Musk with Borneol group was significantly higher than that of themodel group (P<0.05) and the synapse form was almost normal.

模型组较假手术组神经毡内突触明显减少(P<0.01),典型的突触结构遭到破坏;麝香配伍冰片组突触数量较模型组明显增多(P<0.05),突触形态大部分接近正常。

We present a phenomenological description of a two-component process for synaptic plasticity and dynamical model.

我们给出了突触可塑性的ltp和ltd合成的过程、动力学模型及突触增强变化的预测模型,当用预测尖峰的不同频率训练和poisson分布训练时,将产生不同的突触前和突触后的平均电压。

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