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来自内侧隔区的培养神经元中的钙升高会引发周围胶质细胞中的钙波。

Calcium rise in cultured neurons from medial septum elicits calcium waves in surrounding glial cells.

作者信息

Rizzoli Silvio, Sharma Geeta, Vijayaraghavan Sukumar

机构信息

Department of Physiology and Biophysics, and the Neuroscience Program, University of Colorado Health Sciences Center, Denver, CO 80262, USA.

出版信息

Brain Res. 2002 Dec 13;957(2):287-97. doi: 10.1016/s0006-8993(02)03618-1.

Abstract

One prerequisite for understanding the physiological relevance of intercellular calcium waves in glia is the examination of mechanisms that trigger these waves. Here, we show that stimulation of cultured septal neurons to produce a large and sustained calcium rise in the soma can initiate calcium waves in surrounding glial cells. The initiation of calcium waves is dependent on calcium influx through voltage-gated calcium channels on the neuron. The waves are not due to direct stimulation of the glial cells or to loss of neuronal membrane integrity. Mechanism of wave initiation is distinct from that involved in wave propagation and does not involve glutamate or acetylcholine release. Communication via gap junctions, or nitric oxide production, is not involved in the initial signaling between a stimulated neuron and the surrounding astrocytes. Suramin, a blocker of P2 receptors blocked the waves but failed to abolish the responses in glial cells immediately surrounding the stimulated neuron. Our results suggest that patterns of calcium rises on neurons, like those seen in glutamate cytotoxicity, can cause calcium waves in surrounding glial cells.

摘要

理解神经胶质细胞中细胞间钙波的生理相关性的一个前提条件是研究触发这些钙波的机制。在此,我们表明,刺激培养的隔区神经元使其胞体产生大量且持续的钙升高,可引发周围神经胶质细胞中的钙波。钙波的引发依赖于通过神经元上电压门控钙通道的钙内流。这些钙波并非由于对神经胶质细胞的直接刺激或神经元膜完整性的丧失。波引发的机制与波传播所涉及的机制不同,且不涉及谷氨酸或乙酰胆碱的释放。通过缝隙连接的通讯或一氧化氮的产生,并不参与受刺激神经元与周围星形胶质细胞之间的初始信号传递。苏拉明,一种P2受体阻滞剂,可阻断钙波,但未能消除紧邻受刺激神经元的神经胶质细胞中的反应。我们的结果表明,神经元上的钙升高模式,如同在谷氨酸细胞毒性中所见的那样,可导致周围神经胶质细胞中的钙波。

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