Rom-Glas A, Sandler C, Kirschfeld K, Minke B
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
J Gen Physiol. 1992 Nov;100(5):767-81. doi: 10.1085/jgp.100.5.767.
Ion-selective calcium microelectrodes were inserted into the compound eyes of the wild-type sheep blowfly Lucilia or into the retina of the no steady state (nss) mutant of Lucilia. These electrodes monitored light-induced changes in the extracellular concentration of calcium (delta[Ca2+]o) together with the extracellularly recorded receptor potential. Prolonged dim lights induced a steady reduction in [Ca2+]o during light in the retina of normal Lucilia, while relatively little change in [Ca2+]o was observed in the retina of the nss mutant. Prolonged intense light induced a multiphasic change in [Ca2+]o: the [Ca2+]o signal became transient, reaching a minimum within 6 s after light onset, and then rose to a nearly steady-state phase below the dark concentration. When lights were turned off, a rapid increase in [Ca2+]o was observed, reaching a peak above the dark level and then declining again to the dark level within 1 min. In analogy to similar studies conduced in the honeybee drone, we suggest that the reduction in [Ca2+]o reflects light-induced Ca2+ influx into the photoreceptors, while the subsequent increase in [Ca2+]o reflects the activation of the Na-Ca exchange which extrudes Ca2+ from the cells. In the nss mutant in response to intense prolonged light, the receptor potential declines to baseline during light while the Ca2+ signal is almost abolished, revealing only a short transient reduction in [Ca2+]o. Application of lanthanum (La3+), but not nickel (Ni2+), into the retinal extracellular space of normal Lucilia mimicked the effect of the nss mutation on the receptor potential, while complete elimination of the Ca2+ signal in a reversible manner was observed. The results suggest that La3+ and the nss mutation inhibit light-induced Ca2+ influex into the photoreceptor in a manner similar to the action of the trp mutation in Drosophila, which has been shown to block specifically a light-activated Ca2+ channel necessary to maintain light excitation.
将离子选择性钙微电极插入野生型绵羊绿蝇丽蝇的复眼中，或插入丽蝇非稳态（nss）突变体的视网膜中。这些电极监测光诱导的细胞外钙浓度变化（δ[Ca2+]o）以及细胞外记录的感受器电位。长时间的暗光会导致正常丽蝇视网膜在光照期间[Ca2+]o持续降低，而在nss突变体的视网膜中观察到[Ca2+]o变化相对较小。长时间的强光会诱导[Ca2+]o发生多相变化：[Ca2+]o信号变得短暂，在光照开始后6秒内达到最小值，然后上升到低于暗浓度的近稳态阶段。当光照关闭时，观察到[Ca2+]o迅速增加，达到高于暗水平的峰值，然后在1分钟内再次下降到暗水平。与对蜜蜂雄蜂进行的类似研究类似，我们认为[Ca2+]o的降低反映了光诱导的Ca2+流入光感受器，而随后[Ca2+]o的增加反映了将Ca2+从细胞中挤出的钠钙交换的激活。在nss突变体中，对长时间强光的反应是，感受器电位在光照期间降至基线，而Ca2+信号几乎消失，仅显示[Ca2+]o有短暂的瞬时降低。将镧（La3+）而非镍（Ni2+）应用于正常丽蝇的视网膜细胞外空间，模拟了nss突变对感受器电位的影响，同时观察到Ca2+信号以可逆方式完全消除。结果表明，La3+和nss突变以类似于果蝇trp突变的作用方式抑制光诱导的Ca2+流入光感受器，trp突变已被证明能特异性阻断维持光激发所必需的光激活Ca2+通道。
