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pubmed-article:1961249pubmed:abstractTextCALCIUM is involved in the adaptation of vertebrate photoreceptors to light and may have a similar role in invertebrate phototransduction. But the molecular mechanisms mediating this stimulus-dependent regulation are not well understood in any G protein-coupled transduction system. We have developed a preparation of isolated Drosophila photoreceptors that has allowed us to carry out an electrophysiological characterization of the light-activated response in these sensory neurons using patch-clamp techniques. We report here that extracellular calcium entering through the light-activated conductance is a key regulator of both the activation and deactivation phases of the phototransduction cascade, and that inaC mutant photoreceptors are specifically defective in the calcium-dependent deactivation mechanism. These data suggest that the light-dependent calcium influx inactivates this cascade through a biochemical pathway that requires the inaC gene product, and that this mechanism represents a molecular basis for stimulus-dependent regulation of visual transduction in Drosophila photoreceptors.lld:pubmed
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pubmed-article:1961249pubmed:articleTitleA Drosophila mutant defective in extracellular calcium-dependent photoreceptor deactivation and rapid desensitization.lld:pubmed
pubmed-article:1961249pubmed:affiliationHoward Hughes Medical Institute, San Diego, La Jolla, California.lld:pubmed
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