中文摘要：

把烟碱的醋胆素受体(nAChRs ) 基于形成功能的 neuronal 的五个子单元的作文，他们被组织进任何一个 heteromeric (包括伪和尾子单元) 或 homomeric (包括的仅仅伪子单元) 受体。nAChRs 被知道是对钙离子可渗透的差别，与有到钙的最高的渗透之一的伪 7 nAChR 子类型。通过 nAChRs 的钙流入，特别地通过伪 -bungarotoxin 敏感的伪 7 包含 nAChRs，是提起细胞质的钙层次的一个很有效的方法。nAChRs 的激活能调停细胞质的钙信号的三种类型：( 1 )通过 nAChRs 指导钙流入，( 2 )通过被 调停nAChR 的去极激活的电压依赖者钙隧道( VDCC )的间接的钙流入，并且( 3 )导致钙的钙版本( CICR )(由开始的二来源被触发)从 endoplasmic 蜂窝胃(嗯)通过 ryanodine 受体和肌醇( 1,4,5 ) -triphosphate 受体( IP3Rs )。下游的发信号事件由 调停nAChR 的钙回答调停了能被组织进即时效果(例如 neurotransmitter 版本，能在 nAChR 激活以后发生在毫秒，短期的效果(例如 nAChR 的恢复，通过细胞的发信号的不敏感性串联)，并且长期的效果(例如经由基因表示的 neuroprotection )。另外， nAChR 活动能被细胞质的钙层次调整，建议一种复杂相互的关系。在为 neuronal nAChRs 的成像技术，动物模型，和更多的有势力和子类型选择的 ligands 的进一步的进展将在理解 neuronal 帮助发信号的调停 nAChR 的钙，并且导致改进治疗学的处理的发展。

英文摘要：

Based on the composition of the five subunits forming functional neuronal nicotinic acetylcholine receptors （nAChRs）, they are grouped into either heteromeric （comprising both a and β subunits） or homomeric （comprising only a subunits） receptors. The nAChRs are known to be differentially permeable to calcium ions, with the α7 nAChR subtype having one of the highest permeabilities to calcium. Calcium influx through nAChRs, particularly through the a-bungarotoxin-sensitive α7-containing nAChRs, is a very efficient way to raise cytoplasmic calcium levels. The activation of nAChRs can mediate three types of cytoplasmic calcium signals： （1） direct calcium influx through the nAChRs, （2） indirect calcium influx through voltage-dependent calcium channels （VDCCs） which are activated by the nAChR-mediated depolarization, and （3） calciuminduced calcium release （CICR） （triggered by the first two sources） from the endoplasmic reticulum （ER） through the ryanodine receptors and inositol （1,4,5）-triphosphate receptors （IP3Rs）. Downstream signaling events mediated by nAChR- mediated calcium responses can be grouped into instantaneous effects （such as neurotransmitter release, which can occur in milliseconds after nAChR activation）, short-term effects （such as the recovery of nAChR desensitization through cellular signaling cascades）, and long-term effects （such as neuroprotection via gene expression）. In addition, nAChR activity can be regulated by cytoplasmic calcium levels, suggesting a complex reciprocal relationship. Further advances in imaging techniques, animal models, and more potent and subtype-selective ligands for neuronal nAChRs would help in understanding the neuronal nAChR-mediated calcium signaling, and lead to the development of improved therapeutic treatments.