Wässle H, Peichl L, Airaksinen M S, Meyer M
Max-Planck-Institut für Hirnforschung, Neuroanatomie, Deutschordenstrasse 46, D-60528 Frankfurt a.M., Germany.
Cell Tissue Res. 1998 May;292(2):211-8. doi: 10.1007/s004410051052.
Calcium-binding proteins are abundantly expressed in many neurons of mammalian retinae. Their physiological roles are, however, largely unknown. This is particularly true for calcium-modulating proteins ("calcium buffers") such as calbindin D28k. Here, we have studied retinae of wildtype (+/+) and calbindin-null mutant (-/-) mice by using immunocytochemical methods. Although calbindin immunoreactivity was completely absent in the calbindin (-/-) retinae, those cells that express the protein in wildtype retinae, such as horizontal cells, were still present and appeared normal. This was verified by immunostaining horizontal cells for various neurofilament proteins. In order to assess whether other calcium-binding proteins are upregulated in the mutant mouse and may thus compensate for the loss of calbindin, mouse retinae were also immunolabeled for parvalbumin, calretinin, and a calmodulin-like protein (CALP). In no instance could a change in the expression pattern of these proteins be detected by immunocytochemical methods. Thus, our results show that calbindin is not required for the maintenance of the light-microscopic structure of the differentiated retina and suggest roles for this protein in retinal function.
钙结合蛋白在哺乳动物视网膜的许多神经元中大量表达。然而，它们的生理作用在很大程度上尚不清楚。对于诸如钙结合蛋白D28k之类的钙调节蛋白（“钙缓冲蛋白”）而言尤其如此。在这里，我们通过免疫细胞化学方法研究了野生型（+/+）和钙结合蛋白缺失型突变体（-/-）小鼠的视网膜。尽管在钙结合蛋白（-/-）视网膜中完全没有钙结合蛋白免疫反应性，但那些在野生型视网膜中表达该蛋白的细胞，如水平细胞，仍然存在且看起来正常。通过对各种神经丝蛋白对水平细胞进行免疫染色来证实这一点。为了评估其他钙结合蛋白在突变小鼠中是否上调并因此可能补偿钙结合蛋白的缺失，还对小鼠视网膜进行了小白蛋白、钙视网膜蛋白和一种钙调蛋白样蛋白（CALP）的免疫标记。通过免疫细胞化学方法在任何情况下都未检测到这些蛋白表达模式的变化。因此，我们的结果表明，钙结合蛋白对于维持分化视网膜的光学显微镜结构不是必需的，并提示该蛋白在视网膜功能中的作用。
