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突触诱发的星形胶质细胞钙信号特性揭示了星形胶质细胞对突触信息的处理。

Properties of synaptically evoked astrocyte calcium signal reveal synaptic information processing by astrocytes.

作者信息

Perea Gertrudis, Araque Alfonso

机构信息

Instituto Cajal, Consejo Superior de Investigaciones Científicas, Madrid 28002, Spain.

出版信息

J Neurosci. 2005 Mar 2;25(9):2192-203. doi: 10.1523/JNEUROSCI.3965-04.2005.

DOI:10.1523/JNEUROSCI.3965-04.2005
PMID:15745945
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6726085/
Abstract

The synaptic control of the astrocytic intracellular Ca2+ is crucial in the reciprocal astrocyte-neuron communication. Using electrophysiological and Ca2+ imaging techniques in rat hippocampal slices, we investigated the astrocytic Ca2+ signal modulation induced by synaptic terminals that use glutamate and acetylcholine. Ca2+ elevations were evoked by glutamate released from Schaffer collaterals and by acetylcholine, but not glutamate, released by alveus stimulation, indicating that astrocytes discriminate the activity of different synapses belonging to different axon pathways. The Ca2+ signal was modulated bidirectionally by simultaneous activation of both pathways, being depressed at high stimulation frequencies and enhanced at low frequencies. The Ca2+ modulation was attributable to astrocytic intrinsic properties, occurred at discrete regions of the processes, and controlled the intracellular expansion of the Ca2+ signal. In turn, astrocyte Ca2+ signal elicited NMDA receptor-mediated currents in pyramidal neurons. Therefore, because astrocytes discriminate and integrate synaptic information, we propose that they can be considered as cellular elements involved in the information processing by the nervous system.

摘要

星形胶质细胞内Ca2+的突触控制在星形胶质细胞与神经元的相互通讯中至关重要。利用大鼠海马切片中的电生理和Ca2+成像技术,我们研究了使用谷氨酸和乙酰胆碱的突触终末诱导的星形胶质细胞Ca2+信号调制。从Schaffer侧支释放的谷氨酸以及从海马槽刺激释放的乙酰胆碱(而非谷氨酸)均可诱发Ca2+升高,这表明星形胶质细胞能够区分属于不同轴突通路的不同突触的活动。通过同时激活这两条通路,Ca2+信号受到双向调制,在高刺激频率下受到抑制,在低频率下增强。Ca2+调制归因于星形胶质细胞的固有特性,发生在突起的离散区域,并控制Ca2+信号在细胞内的扩展。反过来,星形胶质细胞Ca2+信号在锥体神经元中引发NMDA受体介导的电流。因此,由于星形胶质细胞能够区分和整合突触信息,我们提出它们可被视为参与神经系统信息处理的细胞元件。

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