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.
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1 November 1992
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November 01 1992
The nss mutation or lanthanum inhibits light-induced Ca2+ influx into fly photoreceptors.
A Rom-Glas,
A Rom-Glas
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
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C Sandler,
C Sandler
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
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K Kirschfeld,
K Kirschfeld
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
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B Minke
B Minke
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
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A Rom-Glas
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
C Sandler
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
K Kirschfeld
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
B Minke
Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
Online ISSN: 1540-7748
Print ISSN: 0022-1295
J Gen Physiol (1992) 100 (5): 767–781.
Citation
A Rom-Glas, C Sandler, K Kirschfeld, B Minke; The nss mutation or lanthanum inhibits light-induced Ca2+ influx into fly photoreceptors.. J Gen Physiol 1 November 1992; 100 (5): 767–781. doi: https://doi.org/10.1085/jgp.100.5.767
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