Invertebrate photoreceptors use the inositol-lipid signaling cascade for phototransduction. A useful approach to dissect this pathway and its regulation has been provided by the isolation of Drosophila visual mutants. We measured extracellular changes of Ca 2+ [ACa2+]o in Drosophila retina using CaZ+-selective microelectrodes in both the transient receptor potential (trp) mutant, in which the calcium permeability of the light-sensitive channels is greatly diminished and in the inactivation-but-no-afterpotential C (inaC) mutant which lacks photoreceptor-specific protein kinase C (PKC). Illumination induced a decrease in extracellular [Ca 2+] with kinetics and magnitude that changed with light intensity. Compared to wildtype, the light-induced decrease in [Ca2+]o (the Ca 2+ signal) was diminished in trp but significantly enhanced in inaC. The enhanced Ca 2+ signal was diminished in the double mutant inaC;trp indicating that the effect of the trp mutation overrides the enhancement observed in the absence of eye-PKC. We suggest that the decrease in [CaZ+]o reflects light-induced Ca 2+ influx into the photoreceptors and that the trp mutation blocks a large fraction of this Ca 2+ influx, while the absence of eye specific PKC leads to enhancement of light-induced Ca 2 § influx. This suggestion was supported by Ca 2 § measurements in isolated ommatidia loaded with the fluorescent Ca 2 § indicator, Ca Green-5N, which indicated an approximately threefold larger light-induced increase in cellular Ca 2 § in inaC relative to WT. Our observations are consistent with the hypothesis that TRP is a light activated Ca 2+ channel and that the increased Ca 2 § influx observed in the absence of PKC is mediated mainly via the TRP channel.

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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 (ms) mutant of Lucilia. These electrodes monitored light-induced changes in the extracellular concentration of calcium (A[Ca2+] 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 rain. In analogy to similar studies conduced in the honeybee drone, we suggest that the reduction in [Ca2÷]o reflects light-induced Ca 2÷ influx into the photoreceptors, while the subsequent increase in [Ca~÷]o reflects the activation of the Na-Ca exchange which extrudes Ca ~+ from the cells. In the ms mutant in response to intense prolonged light, the receptor potential declines to baseline during light while the Ca 2+ signal is almost abolished, revealing only a short transient reduction in [Ca~+]o. Application of lanthanum (LaSt), but not nickel (Ni2+), into the retinal extracellular space of normal Lucilia mimicked the effect of the ms mutation on the receptor potential, while complete elimination of the Ca ~+ signal in a reversible manner was observed. The results suggest that La 3+ and the ms mutation inhibit light-induced Ca ~+ influx 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 Ca 2+ channel necessary to maintain light excitation.

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