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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Calcium increases in retinal glial cells evoked by light-induced neuronal activity.
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Calcium increases in retinal glial cells evoked by light-induced neuronal activity.

机译：光诱导的神经元活动引起的视网膜胶质细胞中钙的增加。

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摘要

Electrical stimulation of neurons in brain slices evokes increases in cytoplasmic Ca(2+) in neighboring astrocytes. The present study tests whether similar neuron-to-glial signaling occurs in the isolated rat retina in response to light stimulation. Results demonstrate that Muller cells, the principal retinal glial cells, generate transient increases in Ca(2+) under constant illumination. A flickering light stimulus increases the occurrence of these Ca(2+) transients. Antidromic activation of ganglion cell axons also increases the generation of Muller cell Ca(2+) transients. The increases in Ca(2+) transients evoked by light and antidromic stimulation are blocked by the purinergic antagonist suramin and by TTX. The addition of adenosine greatly potentiates the response to light, with light ON evoking large Ca(2+) increases in Muller cells. Suramin, apyrase (an ATP-hydrolyzing enzyme), and TTX substantially reduce the adenosine-potentiated response. NMDA, metabotropic glutamate, GABA(B), and muscarinic receptor antagonists, in contrast, are mainly ineffective in blocking the response. Light-evoked Ca(2+) responses begin in Muller cell processes within the inner plexiform (synaptic) layer of the retina and then spread into cell endfeet at the inner retinal surface. These results represent the first demonstration that Ca(2+) increases in CNS glia can be evoked by a natural stimulus (light flashes). The results suggest that neuron-to-glia signaling in the retina is mediated by neuronal release of ATP, most likely from amacrine and/or ganglion cells, and that the response is augmented under pathological conditions when adenosine levels increase.
机译：脑切片中神经元的电刺激引起邻近星形胶质细胞的细胞质Ca（2+）增加。本研究测试了在分离的大鼠视网膜中是否响应光刺激发生了类似的神经元到神经胶质信号。结果表明，穆勒细胞，主要的视网膜神经胶质细胞，在恒定光照下在Ca（2+）中产生瞬时增加。闪烁的光刺激增加了这些Ca（2+）瞬变的发生。神经节细胞轴突的反drodromic激活还增加了穆勒细胞Ca（2+）瞬变的生成。嘌呤能拮抗剂苏拉明和TTX阻止了由光和抗皮肤刺激引起的Ca（2+）瞬变的增加。腺苷的添加大大增强了对光的响应，随着光的激发，穆勒细胞中的Ca（2+）增大。苏拉明，腺苷三磷酸酶（一种ATP水解酶）和TTX大大降低了腺苷增强的反应。相比之下，NMDA，代谢型谷氨酸，GABA（B）和毒蕈碱受体拮抗剂在阻止反应方面主要无效。诱发光的Ca（2+）响应开始于视网膜内部丛状（突触）层内的穆勒细胞过程中，然后传播到视网膜内表面的细胞末端。这些结果代表了第一个证明，CNS胶质细胞中Ca（2+）的增加可以由自然刺激引起（闪烁）。结果表明，视网膜中神经元到神经胶质细胞的信号传导是由ATP的神经元释放介导的，最有可能来自无长突神经节细胞和/或神经节细胞，并且在腺苷水平升高的病理条件下反应增强。

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