Microheterogeneity of calcium signalling in dendrites.

Microheterogeneity of calcium signalling in dendrites.
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树突中钙信号传导的微观异质性。

DOI:
10.1111/j.1469-7793.2000.t01-1-00053.x
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发表时间:
2000
期刊:
The Journal of physiology
影响因子:
--
通讯作者:
Andrews,SB
Andrews,SB
中科院分区:
--
文献类型:
--
作者:
Pozzo-Miller,LD;Connor,JA;Andrews,SB

文献摘要

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细胞内游离 Ca2+([Ca2+]i) 浓度的瞬时变化源自电压门控或配体门控流入以及细胞内储存的配体门控或 Ca2+门控释放,触发或调节许多基本神经元过程,包括神经递质释放和突触可塑性。在参与 Ca2+ 清除的细胞内区室中,内质网 (ER) 受到了最多的关注,因为它表达 Ca2+ 泵和 Ca2+ 通道,从而赋予其作为细胞内钙吸收和储存的潜力。我们在此回顾我们正在进行的关于钙封入内质网池和从内质网池释放的作用的研究,以及钙在突触活动期间和之后海马切片锥体神经元树突中游离[Ca2+]i瞬态的产生和终止中所起的作用。这些研究是通过将游离胞质 [Ca2+]i 瞬态的并行微荧光测量与电子显微镜水平上特定树突室内总 Ca 含量的能量色散 X 射线微分析测量相结合来进行的。我们的观察支持了新的认识,即树突状内质网池的特定子集提供了 Ca2+ 信号传导的空间和时间微观异质性,不仅作为主要的细胞内 Ca2+ 汇,参与电压和配体门控 Ca2+ 流入后的主动清除机制,而且还作为细胞内 Ca2+ 源,可以通过源自激活突触的信号级联来动员。
Transient changes in the intracellular concentration of free Ca2+([Ca2+]i) originating from voltage‐ or ligand‐gated influx and by ligand‐ or Ca2+‐gated release from intracellular stores, trigger or modulate many fundamental neuronal processes, including neurotransmitter release and synaptic plasticity. Of the intracellular compartments involved in Ca2+clearance, the endoplasmic reticulum (ER) has received the most attention because it expresses Ca2+pumps and Ca2+channels, thus endowing it with the potential to act as both an intracellular calcium sink and store. We review here our ongoing work on the role of calcium sequestration into, and release from, ER cisterns and the role that this plays in the generation and termination of free [Ca2+]itransients in dendrites of pyramidal neurons in hippocampal slices during and after synaptic activity. These studies have been approached by combining parallel microfluorometric measurements offreecytosolic [Ca2+]itransients with energy‐dispersive X‐ray microanalytical measurements oftotalCa content within specific dendritic compartments at the electron microscopy level. Our observations support the emerging realization that specific subsets of dendritic ER cisterns provide spatial and temporal microheterogeneity of Ca2+signalling, acting not only as a major intracellular Ca sink involved in active clearance mechanisms after voltage‐ and ligand‐gated Ca2+influx, but also as an intracellular Ca2+source that can be mobilized by a signal cascade originating at activated synapses.