权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Regulation of gap junctions by intracellular messengers in retinal neurons

视网膜神经元细胞内信使对间隙连接的调节

基本信息

批准号：
04670083
负责人：
MIYACHI Ei-ichi
金额：
$ 1.34万
依托单位：
Fujita Health University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1992
资助国家：
日本
起止时间：
1992 至 1993
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-04670083/
关键词：
Retina Horizontal cell Gap junction Intracellular messenger Cyclic GMP Guanylate cyclase Nitric oxide (NO)Arachidonic acid ギャップ・ジャンクション環状AMP

项目摘要

1. Horizontal cells in carp and turtle retinas are electrically coupled through gap junctions, and the input resistance of the cells is too low to be measured. However, the input resistance was significantly increased after injection of L-arginine, known as the precursor of nitric oxide (NO), or arachidonic acid into horizontal cells. Intracellular injection of these chemicals also blocked dye-coupling of Lucifer Yellow CH among horizontal cells.2. On the other hand, dye-coupling was observed when the mixture of L- arginine and an NO synthase inhibitor, such as N^G-monomethyl-L-arginine and N^G-nitro-L-arginine, was injected into horizontal cells. Injection of a soluble guanylate cyclase inhibitor, such as methylene blue and cystamine, also suppressed the decoupling effect of L-arginine.3. Dye-coupling was observed when nordihydroguaiaretic acid (NDGA), a lipoxygenase inhibitor, was injected into the cells, together with arachidonic acid. Injection of methylene blue or cystamine also suppressed the decoupling effect of arachidonic acid. On the other hand, dye-coupling was eliminated when indomethacin, a cyclo-oxygenase inhibitor, was injected into horizontal cells, together with arachidonic acid. And injection of the mixture of arachidonic acid and indomethacin caused significant increase in the input resistance of horizontal cells.4. These results suggest that nitric oxide (NO) and lipoxygenase metabolites of arachidonic acid block gap junctions between retinal neurons, and that the decoupling effects are induced by activating guanylate cyclase.

1.鲤鱼和甲鱼视网膜的水平细胞通过缝隙连接进行电耦合，细胞的输入电阻太低，无法测量。然而，将被称为一氧化氮(NO)前体的L精氨酸或花生四烯酸注入水平细胞后，输入阻力显著增加。这些化学物质的细胞内注射也阻止了荧光黄CH在水平细胞之间的染料偶联。而将L-精氨酸与一氧化氮合酶抑制剂N^G-单甲基-L-精氨酸和N^G-硝基-L-精氨酸的混合物注入水平细胞，则观察到染料偶联现象。注射可溶性鸟苷环化酶抑制剂，如亚甲蓝和半胱胺，也可抑制L-精氨酸的去偶联作用。当脂肪氧合酶抑制剂去甲二氢愈创木酸(NDGA)与花生四烯酸一起注入细胞内时，观察到染料偶联。注射亚甲蓝或半胱胺也可抑制花生四烯酸的解偶联作用。另一方面，将环氧合酶抑制剂吲哚美辛与花生四烯酸一起注入水平细胞，可消除染料偶联。注射花生四烯酸和吲哚美辛混合液后，水平细胞的输入阻力明显增加。这些结果表明，花生四烯酸的一氧化氮(NO)和脂氧合酶代谢产物阻断了视网膜神经元之间的缝隙连接，这种解偶联作用是通过激活鸟苷环化酶来诱导的。