Light-induced extracellular calcium and sodium concentration changes in the retina of Calliphora: involvement in the mechanism of light adaptation

Sandler, C.; Kirschfeld, K

doi:10.1007/bf00206994

Cited by 22 publications

(33 citation statements)

References 70 publications

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“…17). Electrophysiological analyses indicate that the depolarization drop from the peak to the plateau value is due to down-regulation of the receptor gain by the increased intracellular calcium concentration (Sandier and Kirschfeld, 1991). The intensity range of mitochondrial activation appears to correspond with the range where peak and plateau deviate.…”

Section: Pumps and Channelsmentioning

confidence: 92%

Insect retinal pigments: Spectral characteristics and physiological functions

Stavenga

1995

Progress in Retinal and Eye Research

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Section: Pumps and Channelsmentioning

confidence: 92%

Insect retinal pigments: Spectral characteristics and physiological functions

Stavenga

1995

Progress in Retinal and Eye Research

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“…Extracellular Ca 2ϩ enters the photoreceptors through ion channels and is required for rapid recovery of visual excitation (1)(2)(3)(4)(5). A major portion of the Ca 2ϩ influx into the photoreceptor cell appears to be carried by a Ca 2ϩ -selective class of channels that depend on, or may indeed be formed by, the transient receptor potential (trp) 1 protein (6,7).…”

mentioning

confidence: 99%

Phosphorylation of the InaD Gene Product, a Photoreceptor Membrane Protein Required for Recovery of Visual Excitation

Huber

Sander

Paulsen

1996

Journal of Biological Chemistry

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In an approach directed to isolate and characterize key proteins of the transduction cascade in photoreceptors using the phosphoinositide signaling pathway, we have isolated the Calliphora homolog of the Drosophila InaD gene product, which in Drosophila InaD mutants causes slow deactivation of the light response. By screening a retinal cDNA library with antibodies directed against photoreceptor membrane proteins, we have isolated a cDNA coding for an amino acid sequence of 665 residues (M r ‫؍‬ 73,349). The sequence displays 65.3% identity (77.3% similarity) with the Drosophila InaD gene product. Probing Western blots with monospecific antibodies directed against peptides comprising amino acids 272-542 (anti-InaD-(272-542)) or amino acids 643-655 (anti-InaD-(643-655)) of the InaD gene product revealed that the Calliphora InaD protein is specifically associated with the signal-transducing rhabdomeral photoreceptor membrane from which it can be extracted by high salt buffer containing 1.5 M NaCl. As five out of eight consensus sequences for protein kinase C phosphorylation reside within stretches of 10 -16 amino acids that are identical in the Drosophila and Calliphora InaD protein, the InaD gene product is likely to be a target of protein kinase C. Phosphorylation studies with isolated rhabdomeral photoreceptor membranes followed by InaD immunoprecipitation revealed that the InaD protein is a phosphoprotein. In vitro phosphorylation is, at least to some extent, Ca 2؉ -dependent and activated by phorbol 12-myristate 13-acetate. The inaC-encoded eye-specific form of a protein kinase C (eye-PKC) is co-precipitated by antibodies specific for the InaD protein from detergent extracts of rhabdomeral photoreceptor membranes, suggesting that the InaD protein and eye-PKC are interacting in these membranes. Co-precipitating with the InaD protein and eye-PKC are two other key components of the transduction pathway, namely the trp protein, which is proposed to form a Ca 2؉ channel, and the norpA-encoded phospholipase C, the primary target enzyme of the transduction pathway. It is proposed that the rise of the intracellular Ca 2؉ concentration upon visual excitation initiates the phosphorylation of the InaD protein by eye-PKC and thereby modulates its function in the control of the light response.

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“…The extracellular K + activity was measured in the fly retina using K + -selective double-barreled microelectrodes, which were fabricated as previously described (Sandler and Kirschfeld, 1991; Semb et al, 1997). Briefly, a K + -selective microelectrode was pulled from the borosilicate double-barreled capillaries with a filament.…”

Section: Methodsmentioning

confidence: 99%

Loss of Na+/K+-ATPase in Drosophila photoreceptors leads to blindness and age-dependent neurodegeneration

Zhuo

Reddig

2014

Experimental Neurology

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The activity of Na+/K+-ATPase establishes transmembrane ion gradients and is essential to cell function and survival. Either dysregulation or deficiency of neuronal Na+/K+-ATPase has been implicated in the pathogenesis of many neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease and rapid-onset dystonia Parkinsonism. However, genetic evidence that directly links neuronal Na+/K+-ATPase deficiency to in vivo neurodegeneration has been lacking. In this study, we use Drosophila photoreceptors to investigate the cell-autonomous effects of neuronal Na+/K+ ATPase. Loss of ATPα, an α subunit of Na+/K+-ATPase, in photoreceptors through UAS/Gal4-mediated RNAi eliminated the light-triggered depolarization of the photoreceptors, rendering the fly virtually blind in behavioral assays. Intracellular recordings indicated that ATPα knockdown photoreceptors were already depolarized in the dark, which was due to a loss of intracellular K+. Importantly, ATPα knockdown resulted in the degeneration of photoreceptors in older flies. This degeneration was independent of light and showed characteristics of apoptotic/hybrid cell death as observed via electron microscopy analysis. Loss of Nrv3, a Na+/K+-ATPase β subunit, partially reproduced the signaling and degenerative defects observed in ATPα knockdown flies. Thus, loss of Na+/K+-ATPase not only eradicates visual function but also causes age-dependent degeneration in photoreceptors, confirming the link between neuronal Na+/K+ ATPase deficiency and in vivo neurodegeneration. This work also establishes Drosophila photoreceptors as a genetic model for studying the cell-autonomous mechanisms underlying neuronal Na+/K+ ATPase deficiency-mediated neurodegeneration.

show abstract

Light-induced extracellular calcium and sodium concentration changes in the retina of Calliphora: involvement in the mechanism of light adaptation

Cited by 22 publications

References 70 publications

Insect retinal pigments: Spectral characteristics and physiological functions

Insect retinal pigments: Spectral characteristics and physiological functions

Phosphorylation of the InaD Gene Product, a Photoreceptor Membrane Protein Required for Recovery of Visual Excitation

Loss of Na+/K+-ATPase in Drosophila photoreceptors leads to blindness and age-dependent neurodegeneration

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