尼古丁受体

高表达APP转基因小鼠脑组织中α7尼古丁受体蛋白水平升高49%；

High level of alpha-7 nAChR protein was also observed in mouse brain tissues with APP mutation .

用蛋白印记方法测定α3和α7尼古丁受体亚单位蛋白水平；用逆转录聚合酶链反应方法测定尼古丁受体亚单位mRNA水平。

The α 3 and α 7 nAChR subunits in protein level were measured by Western blotting and in mRNA level by RT-polymerase chain reaction ( RT-PCR ) .

氟中毒大鼠脑组织和PC12细胞中脂质和尼古丁受体的改变

Changes of lipids and nicotinic receptors in rat brains and Pheochromocytoma with fluorosis

阿尔茨海默病患者神经型尼古丁受体α7亚单位基因多态性：发现一个新的GTG三碱基插入突变

Subunit gene polymorphisms of neural nicotinic receptor alpha 7 in patients with Alzheimer disease : A new GTG tribasic insertion mutation

近年来，基于胆碱能假说，人们将大量的研究集中于寻找高效的、有选择性的AChE抑制剂，从而提高中枢神经系统中蝇碱受体和尼古丁受体处的乙酰胆碱水平。

Presently , in the frame of the so-called " cholinergic hypothesis ", a great deal of research is being devoted to the discovery of the potent and selective AChE inhibitors able to maintain high levels of acetylcholine at the muscarinic and nicotinic receptors in the central nervous system .

精神分裂症患者大脑皮质尼古丁受体亚单位蛋白质水平的改变

Nicotinic Receptor Subunit Proteins in the Cortex of the Patients with Schizophrenia

在你停止吸烟时，你的尼古丁受体不再被启动，因而你无法得到你习惯得到的那么多多巴胺。

When you stop smoking , and your nicotine receptors stop being activated .

当前，在非神经组织（细胞）上考察尼古丁受体及其功能活性，将揭示尼古丁受体的新功能。

Currently , study nAChRs and their function in non-neuro cells will reveal new fuction of nAChRs .

阿尔茨海默病发病机制中β淀粉样蛋白对星形胶质细胞和神经细胞α7尼古丁受体的影响

Effect of beta-amyloid peptides on alpha-7 nicotinic receptor status in astrocytes and neurons , and its relationship to pathogenesis of Alzheimer 's disease

例如，免疫细胞上α7尼古丁受体的阐明，触发人们研究尼古丁受体激动剂对感染和炎症性疾病的治疗学意义。

For example , the clarification of α 7 nicotinic receptor in immune cells triggered the studies on therapeutics significance of nicotinic receptor agonist treating infectious and imflammatory diseases .

目的观察氟中毒对神经细胞中尼古丁受体亚单位蛋白和基因表达水平的影响及氟中毒引起尼古丁受体功能改变的发生机制。

Objective To investigate the influence of fluorosis on nicotinic acetylcholine receptors ( nAChRs ) in protein and gene levels in SH-SY5Y cells and the mechanism of the receptor modification .

最近研究显示，神经型尼古丁受体也可在许多非神经细胞中表达[5,6]，而且，非神经细胞上尼古丁受体及其功能的发现，已经吸引不同领域科学家对这一经典受体产生新的研究兴趣。

Recent studies pointed out that nAChRs are also expressed in many non-neuro cells . Moreover , the fact that nicotine receptors and their function were discovered in non-neuro cells has already attracted scientists in different fields .

外周尼古丁受体阻断剂合并尼古丁治疗并不阻断尼古丁增强胰岛素敏感性的作用，但阻断尼古丁减少血清甘油三酯，说明尼古丁致胰岛素增敏主要经由中枢机制。

Periphery nicotinic receptor blocker plus nicotine treatment did not abolish the insulin sensitivity enhancing effect of nicotine , but abolished the triglyceride lowering effect of nicotine . These indicated that nicotine enhance insulin sensitivity major through central mechanism .

结论氟中毒可引起神经母细胞瘤细胞受损，降低尼古丁受体蛋白水平，其机制与该受体的基因表达水平无关，但与自由基的损害有关。

Conclusion Fluorosis should result in damage of cells and the declined expression of nAChRs in protein levels , but no influences on gene expression of the receptors in human neuroblastoma neurons . The decreased nAChR proteins might be involved in the mechanism of oxidative stress induced by fluorosis .

而确定特定的尼古丁功能受体，对于发挥尼古丁有益的治疗作用意义重大。

Meanwhile , determining specific nicotinic receptor is of most importance for therapeutic use of nicotine .

受影响的基因似乎会产生一种蛋白质，在大脑中发挥尼古丁“受体”或停靠点的作用。

The gene affected seems to make a protein that acts as a " receptor " or docking point for nicotine in the brain .

尼古丁与各种受体结合，促发不同的信号级联反应；

Nicotine can bind to each combination and spur a cascade of distinct events ;

尼古丁是烟碱乙酰胆碱受体（nAChRs）的典型激动剂，具有潜在的治疗中枢神经系统性疾病的作用。

Nicotine is a prototypical agonist of neuronal nicotinic acetylcholine receptors ( nAChRs ) and exerts an important modulatory influence on the CNS .