title: The nss mutation or lanthanum inhibits light-induced Ca2+ influx into fly photoreceptors.
abstract: 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.
authors.affiliation: Department of Physiology Hebrew University, Hadassah Medical School, Jerusalem, Israel.
authors.forename: A
authors.initials: A
authors.lastname: Rom-Glas
authors.forename: C
authors.initials: C
authors.lastname: Sandler
authors.forename: K
authors.initials: K
authors.lastname: Kirschfeld
authors.forename: B
authors.initials: B
authors.lastname: Minke
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects; D004175:Diptera / Q000187:drug effects / Q000235:genetics / Q000378:metabolism*; D007811:Lanthanum / Q000494:pharmacology; D008027:Light; D050356:Lipid Metabolism; D009154:Mutation; D010786:Photoreceptor Cells / Q000187:drug effects / Q000378:metabolism* / Q000528:radiation effects
chemical_list: D015220:Calcium Channels; D007811:Lanthanum; D002118:Calcium