视网膜中神经胶质细胞与神经元之间的对话：神经元兴奋性的调节。
A dialogue between glia and neurons in the retina: modulation of neuronal excitability.
作者信息
Newman Eric A
机构信息
Department of Neuroscience, University of Minnesota, 6-145 Jackson Hall, 321 Church Street SE, Minneapolis, MN 55455, USA.
出版信息
Neuron Glia Biol. 2004 Aug;1(3):245-52. doi: 10.1017/S1740925X0500013X.
Bidirectional signaling between neurons and glial cells has been demonstrated in brain slices and is believed to mediate glial modulation of synaptic transmission in the CNS. Our laboratory has characterized similar neuron-glia signaling in the mammalian retina. We find that light-evoked neuronal activity elicits Ca(2+) increases in Müller cells, which are specialized retinal glial cells. Neuron to glia signaling is likely mediated by the release of ATP from neurons and is potentiated by adenosine. Glia to neuron signaling has also been observed and is mediated by several mechanisms. Stimulation of glial cells can result in either facilitation or depression of synaptic transmission. Release of D-serine from Müller cells might also potentiate NMDA receptor transmission. Müller cells directly inhibit ganglion cells by releasing ATP, which, following hydrolysis to adenosine, activates neuronal A(1) receptors. The existence of bidirectional signaling mechanisms indicates that glial cells participate in information processing in the retina.
神经元与神经胶质细胞之间的双向信号传导已在脑片中得到证实，并且被认为介导了中枢神经系统中神经胶质细胞对突触传递的调节。我们实验室已经对哺乳动物视网膜中类似的神经元 - 神经胶质细胞信号传导进行了表征。我们发现光诱发的神经元活动会引起视网膜特化神经胶质细胞——米勒细胞内钙离子浓度升高。神经元向神经胶质细胞的信号传导可能由神经元释放ATP介导，并被腺苷增强。神经胶质细胞向神经元的信号传导也已被观察到，并且由多种机制介导。刺激神经胶质细胞可导致突触传递的促进或抑制。米勒细胞释放D - 丝氨酸也可能增强NMDA受体传递。米勒细胞通过释放ATP直接抑制神经节细胞，ATP水解为腺苷后会激活神经元的A(1)受体。双向信号传导机制的存在表明神经胶质细胞参与了视网膜中的信息处理。
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