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以前结果表明 ,ryanodine受体 (ryanodinereceptors ,RyRs)门控的咖啡因敏感的钙库和钙引钙释放(Ca2 + inducedCa2 +release ,CICR)机制存在于鲫鱼视网膜ON型双极细胞的胞体中[1] 。采用RyRs的免疫细胞化学方法和细胞内钙测量技术 ,我们进一步研究了RyRs门控的钙库是否存在于这些细胞的轴突末梢中。视网膜纵切和分离细胞的免疫细胞化学研究显示 ,RyRs主要位于ON型双极细胞的胞体中。咖啡因浓度升至 4 0mmol/L在轴突末梢不能诱导钙信号。在细胞外K+浓度升至 10mmol/L引起静息 [Ca2 +]i 轻微升高后 ,咖啡因在轴突末梢也不能诱导钙信号。在forskolin或多巴胺引起细胞内cAMP浓度升高 ,进而cAMP依赖的磷酸化增强后 ,咖啡因在轴突末梢仍不能诱导钙信号。此外 ,50 μmol/Lryanodine对 65mmol/LK+作用 1min或 2min诱导的轴突末梢的钙信号没有产生任何效应。这些结果表明 ,在鲫鱼视网膜ON型双极细胞的轴突末梢中不存在RyRs门控的咖啡因敏感的钙库和CICR机制
Previous results indicated that the caffeine-sensitive calcium stores and Ca2 + -induced Ca2 + release (CICR) mechanisms that are gated by ryanodine receptors (RyRs) are present in the cell bodies of the retina-ON bipolar cells [1 ]. Using RyRs immunocytochemistry and intracellular calcium measurement techniques, we further investigated whether RyRs-gated calcium stores are present in the axonal terminals of these cells. Immunocytochemical studies of retinal sections and isolated cells show that RyRs are predominantly located in the soma of ON bipolar cells. Caffeine concentration increased to 40mmol / L in the axon can not induce calcium signaling. Caffeine also failed to induce calcium signaling at the axonal terminals after extracellular K + concentration was increased to 10 mmol / L causing a slight increase in resting [Ca2 +] i. After forskolin or dopamine caused an increase in intracellular cAMP concentrations, cAMP-dependent phosphorylation was enhanced and caffeine did not induce calcium signaling at axonal terminals. In addition, 50 μmol / Lryanodine did not produce any effect on the calcium signal of axon terminals induced by 65 mmol / L K + for 1 min or 2 min. These results indicate that there is no RyRs-gated caffeine-sensitive calcium pool and CICR mechanism in axon terminals of crucian-reared ON bipolar cells