Endogenous zinc can be a modulator of glycinergic signaling pathway in the rat retina |
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Authors: | Email author" target="_blank">Makoto?KanedaEmail author Katsuyoshi?Ishii Takumi?Akagi Tetsuya?Tatsukawa Tsutomu?Hashikawa |
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Institution: | (1) Department of Physiology, Keio University School of Medicine, Tokyo 160-8582, Japan;(2) Laboratory for Neural Architecture, Brain Science Institute, RIKEN, Wako Saitama, 351-0198, Japan;(3) Laboratory of Cellular Neurobiology School of Life Science, Tokyo University of Pharmacy and Life Science, 1432-1 Horinouchi, Hachioji Tokyo, 192-0392, Japan |
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Abstract: | Summary Zinc is a modulator of glutamatergic inputs in the hippocampus. In the retina, however, we previously reported that endogenous zinc is present in the non-glutamatergic neural processes and earlier electrophysiological studies suggest that zinc is a modulator of inhibitory signaling pathways, which are mediated by glycine and GABA. AII amacrine cells, a subpopulation of glycinergic amacrine cells, are identified by selective immunoreactivity for parvalbumin in the rat retina. In the present study, therefore, we focused on whether zinc is present in AII amacrine cells using silver amplification combined with immunohistochemistry in the rat retina. We also examined whether zinc modulate glycine response in the rat retina by the patch clamp technique. Association of silver precipitates with the parvalbumin-immunoreactive neural processes was observed at the ultrastructural level. We also found that zinc existed in the neural processes which were not parvalbumin-immunoreactive. Glycine-induced responses were augmented when the concentration of Zn2+ was below 10 M, but inhibited at Zn2+ concentrations of 50 M or more. Our results suggest the notion that zinc in neural processes of retinal neurons modulates the inhibitory signaling pathway, particularly that mediated by glycine receptors in AII amacrine cells. |
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