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Calcium imaging demonstrates colocalization of calcium influx and extrusion in fly photoreceptors.

ABSTRACT: During illumination, Ca(2+) enters fly photoreceptor cells through light-activated channels that are located in the rhabdomere, the compartment specialized for phototransduction. From the rhabdomere, Ca(2+) diffuses into the cell body. We visualize this process by rapidly imaging the fluorescence in a cross section of a photoreceptor cell injected with a fluorescent Ca(2+) indicator in vivo. The free Ca(2+) concentration in the rhabdomere shows a very fast and large transient shortly after light onset. The free Ca(2+) concentration in the cell body rises more slowly and displays a much smaller transient. After approximately 400 ms of light stimulation, the Ca(2+) concentration in both compartments reaches a steady state, indicating that thereafter an amount of Ca(2+), equivalent to the amount of Ca(2+) flowing into the cell, is extruded. Quantitative analysis demonstrates that during the steady state, the free Ca(2+) concentration in the rhabdomere and throughout the cell body is the same. This shows that Ca(2+) extrusion takes place very close to the location of Ca(2+) influx, the rhabdomere, because otherwise gradients in the steady-state distribution of Ca(2+) should be measured. The close colocalization of Ca(2+) influx and Ca(2+) extrusion ensures that, after turning off the light, Ca(2+) removal from the rhabdomere is faster than from the cell body. This is functionally significant because it ensures rapid dark adaptation.

SUBMITTER: Oberwinkler J

PROVIDER: S-EPMC26990 | biostudies-literature | 2000 Jul

REPOSITORIES: biostudies-literature

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Calcium imaging demonstrates colocalization of calcium influx and extrusion in fly photoreceptors.

Oberwinkler J J Stavenga D G DG

Proceedings of the National Academy of Sciences of the United States of America 20000701 15

During illumination, Ca(2+) enters fly photoreceptor cells through light-activated channels that are located in the rhabdomere, the compartment specialized for phototransduction. From the rhabdomere, Ca(2+) diffuses into the cell body. We visualize this process by rapidly imaging the fluorescence in a cross section of a photoreceptor cell injected with a fluorescent Ca(2+) indicator in vivo. The free Ca(2+) concentration in the rhabdomere shows a very fast and large transient shortly after light ...[more]

PMID: 10900015

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Project description:Calcium is a key regulator of axon degeneration caused by trauma and disease, but its specific spatial and temporal dynamics in injured axons remain unclear. To clarify the function of calcium in axon degeneration, we observed calcium dynamics in single injured neurons in live zebrafish larvae and tested the temporal requirement for calcium in zebrafish neurons and cultured mouse DRG neurons. Using laser axotomy to induce Wallerian degeneration (WD) in zebrafish peripheral sensory axons, we monitored calcium dynamics from injury to fragmentation, revealing two stereotyped phases of axonal calcium influx. First, axotomy triggered a transient local calcium wave originating at the injury site. This initial calcium wave only disrupted mitochondria near the injury site and was not altered by expression of the protective WD slow (WldS) protein. Inducing multiple waves with additional axotomies did not change the kinetics of degeneration. In contrast, a second phase of calcium influx occurring minutes before fragmentation spread as a wave throughout the axon, entered mitochondria, and was abolished by WldS expression. In live zebrafish, chelating calcium after the first wave, but before the second wave, delayed the progress of fragmentation. In cultured DRG neurons, chelating calcium early in the process of WD did not alter degeneration, but chelating calcium late in WD delayed fragmentation. We propose that a terminal calcium wave is a key instructive component of the axon degeneration program.Significance statementAxon degeneration resulting from trauma or neurodegenerative disease can cause devastating deficits in neural function. Understanding the molecular and cellular events that execute axon degeneration is essential for developing treatments to address these conditions. Calcium is known to contribute to axon degeneration, but its temporal requirements in this process have been unclear. Live calcium imaging in severed zebrafish neurons and temporally controlled pharmacological treatments in both zebrafish and cultured mouse sensory neurons revealed that axonal calcium influx late in the degeneration process regulates axon fragmentation. These findings suggest that temporal considerations will be crucial for developing treatments for diseases associated with axon degeneration.

Dataset Information

Calcium imaging demonstrates colocalization of calcium influx and extrusion in fly photoreceptors.

Publications

Calcium imaging demonstrates colocalization of calcium influx and extrusion in fly photoreceptors.

Similar Datasets

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