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The activation of NRM neurons by electroaeupuncture was eliminated after decerebration at superior colliculus level, indicating that this effect of EA depends mainly on the supra-midbrain structure. Furthermore, all treatments including AR isolation, disconnection of #beta#-endorphinergic tract and micrpinjection of naloxone or anti-#beta#-endorphin serum into PAG, would make the effect of EA disappear. Thus, it is the #beta#-endorphinergic pathway between AR and PAG-NRM system that mediates the major excitatory effect of EA on NRM.

检验AR至 PAG-NRM的神经通路在电针效应中的作用：实验显示上丘水平去大脑后，电针兴奋NRM的效应完全消失，表明此效应主要依赖中脑以上结构实现，进一步分别用Halfisz氏刀游离AR、切断AR至PAG的β-End能束、PAG内注射纳洛酮或抗β-End血清后，也使电针效应基本上完全消失，说明电针使NRM神经元兴奋的效应，主要通过AR与PAG-NRM间的β-End能神经通路实现。

A technology of electrolytic lesion was used to destroy the projections of cerebellar FN neurons to hypothalamus in decussation of superior cerebellar peduncle.

电毁损小脑上脚交叉中顶核投射至下丘脑的神经纤维，然后再用生物素化葡聚糖胺顺行追踪观察小脑顶核-下丘脑之间神经元投射。

In normal group and sham lesion group, BDA positive neurons were distributed symmetrically in the pyramid cells of sensorimotor cortex, and BDA positive fibers of pyramid cells passed through the cerebral cortex, internal capsule, cerebral peduncle of midbrain, basilar portion of pons to the pyramid of medulla oblongata. At the lower part of the medulla oblongata, most of the BDA positive fibers passed through the pyramidal decussation to the contralateral side, continously descended at the ventral part of posterior funiculus just dorsal to the posterior gray commissure and ended at sacral spinal segments.

正常组和假损伤组大鼠BDA示踪显示BDA标记阳性细胞定位于双侧感觉运动皮层的锥体细胞，锥体细胞发出的BDA阳性纤维束对称分布于双侧皮层、内囊、大脑脚、脑桥基底部、延髓锥体中的皮质脊髓束内，继而经锥体交叉到脊髓后索，在双侧后索最深层、灰质后连合背侧下行至脊髓骶段。

Soma and dendrite of NOS neurons were similar in each group.

各组大鼠一氧化氮合酶阳性神经元的胞体和树突均相似。

Between any neurons, between the axon of one neuron and the dendrite of another, there's a tiny gap.

在任何神经之间，在轴突和一个神经以及另一个树突之间，有一个微小的分歧。

A few PV-IR neurons were seen in CA3 and the dentate gyrus until 38 weeks.

直至38周，CA3和齿状回内才可见到少量PV-IR神经元。

The subthreshold oscillations were induced by depolarization in 48% of the recorded neurons.

在本实验中，去极化能诱发阈下振荡的细胞占所记录神经元的48%。

They express widely inperipheral and central nerve system and participate in many important physiological andpathological processes,such as learning and memroy,synaptic plasticity,cerebral ischemiaand pain.Activation of ASICs by protons can depolarize the neurons and generate action potentials.

它广泛分布于中枢及外周神经系统的神经元，参与了很多重要的生理过程和病理反应，与学习记忆、突触可塑性、脑缺血、疼痛等关系密切。H~+激活ASICs可使神经元去极化，产生动作电位，参与了组织酸化如缺血、炎症、肿瘤、癫痫等时痛觉的感受。

The relationship between kainic acid induced death of NOS neurons and vasoconstriction with diaschisis.

急性眼高压大鼠视网膜谷氨酸/天冬氨酸转运体和谷氨酰胺合成酶的表达。

In addition to glial cells, CNTF immunoreactivity are widely localized at neurons in the olfactory bulb, cortex, hippocampus, cerebellum, diencephalon and brainstem.

结果表明，CNTF免疫反应物质除广泛存在于中枢神经系统的胶质细胞外，亦有神经元的广泛染色，而且分布广泛，在嗅脑、大脑皮层、海马、小脑、间脑、脑干中均有明显的染色。

But we don't care about Battlegrounds.

但我们并不在乎沙场中的显露。

Ah! don't mention it, the butcher's shop is a horror.

啊！不用提了。提到肉，真是糟透了。