Na+- and cGMP-induced Ca2+ fluxes in frog rod photoreceptors.

Schnetkamp, Paul P. M.; Bownds, M D

doi:10.1085/jgp.89.3.481

Cited by 33 publications

(17 citation statements)

References 37 publications

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“…3) demonstrate that when [Ca2+]0 is substituted for Ba2+, the slow tails are significantly reduced in magnitude and their decay time is slowed, consistent with a reduced capacity of the exchanger. As expected from previous work in the visual system and in heart (Tibbits & Philipson, 1982;Kimura et al 1987 (Baker & McNaughton, 1976;Yau & Nakatani, 1984;Schnetkamp & Bownds, 1987) suggest that this manoeuvre should inhibit the Na+-Ca2+ exchanger. Our data (Fig.…”

Section: Discussionsupporting

confidence: 75%

“…In the squid axon (Baker & McNaughton, 1976) and in amphibian retina (Yau & Nakatani, 1984;Schnetkamp & Bownds, 1987), fluxes mediated by the Na+-Ca2+ exchanger and currents attributed to its activity can be inhibited by raising [K+]o. Consistent with this we have observed (n = 8) that the slow tail currents were reduced substantially by raising…”

Section: Methodsmentioning

confidence: 99%

“…the retina), which do not exhibit transmembrane ionic currents which overlap and obscure IEX (Yau & Nakatani, 1984;Schnetkamp & Bownds, 1987). In guinea-pig ventricular cells recent evidence strongly suggests that the rise in [Ca2+],, associated with each contraction, triggers this current (Fedida et al 1987).…”

Section: Introductionmentioning

confidence: 99%

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Slow inward tail currents in rabbit cardiac cells.

W¹,

Shimoni²

1989

The Journal of Physiology

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SUMMARY1. A whole-cell gigaseal suction microelectrode voltage-clamp technique has been used to study slow inward tail currents in single myocytes obtained by enzymatic dispersion of rabbit ventricle and atrium. A variety of stimulation protocols, Tyrode solutions and pharmacological agents have been used to test three hypotheses: (a) that the slow inward tail current is generated by an electrogenic Na+-Ca2+ exchanger; (b) that a rise in [Ca2±]1, due to release from the sarcoplasmic reticulum can modulate the activity of this exchanger; and (c) that the uptake of calcium by the sarcoplasmic reticulum is a major determinant of the time course of the tail current.2. As shown previously in amphibian atrium and guinea-pig ventricle, slow inward tail currents can be observed consistently under conditions in which action potentials and ionic currents are recorded using microelectrode constituents which only minimally disturb the intracellular milieu.3. In ventricular cells, the envelope of these tail currents obtained by varying the duration of the preceding depolarizations shows that (a) the tail currents are activated by pulses as short as 10 ms, and reach a maximum for pulse durations of 100-200 ms, (b) the rate of decay of the tail current gradually increases as the activating depolarizations are prolonged, and (c) the tails cannot be due to deactivation of calcium currents, in agreement with other studies in frog heart. 7. The slow tail currents were changed significantly by increasing the temperature of the superfusing Tyrode solution. The major effect was a speeding up of the decay time. This was most apparent for tails following short depolarizations, which normally decay quite slowly at room temperature.8. Caffeine (2-5 mM) produced a prolongation of the decay time of the slow tails, and a small reduction in slow tail amplitudes. The peak of the 'envelope' of the tails was shifted so that it occurred at longer depolarizations.9. In atrial cells, somewhat similar tail currents could be recorded consistently. However, in atrium they decayed much faster and there was very little difference in decay time between short and long depolarizations. Caffeine also prolonged the decay time of these tail currents.10. The slow tail currents in atrial cells are very sensitive to stimulus rate. They were large after short rest periods (30-60 s), and declined to a steady-state level within one to two pulses (at 1-3 Hz) after stimulation was resumed.11. These results from rabbit ventricular and atrial cells support the hypothesis that the slow tail current reflects the electrogenic activity of the Na'-Ca2" exchanger. However, the observed changes in the slow tail currents caused by indirect manipulations of Ca2+ sequestration into the sarcoplasmic reticulum suggest that intracellular calcium homeostasis involves a complex interaction between Ca2+ sequestration into the sarcoplasmic reticulum and Ca2+ extrusion via the Na+-Ca2+exchanger.

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Section: Discussionsupporting

confidence: 75%

Section: Methodsmentioning

confidence: 99%

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Slow inward tail currents in rabbit cardiac cells.

W¹,

Shimoni²

1989

The Journal of Physiology

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“…Intracellular Ca 2+ buffers and sensors are thought to bind as much as 99% of Ca 2+ which enters the cell through CNG channels (47,51). Their action seems to be essential for cell survival, because mutations in genes encoding different photoreceptor Ca 2+ -binding proteins are linked to several human pathologies leading to blindness (52) In addition to plasma membrane Ca 2+ influx and extrusion, [Ca 2+ ]i in the OS may also be regulated by Ca 2+ release and uptake from internal compartments, such as the stack of disks which fill the rod OS (54)(55)(56)(57). Early studies suggested that the disks can accumulate significant amounts of Ca 2+ .…”

Section: Ca 2+ Extrusion and Buffering In The Outer Segmentmentioning

confidence: 99%

Calcium regulation in photoreceptors

2002

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In this review we describe some of the remarkable and intricate mechanisms through which the calcium ion (Ca 2+ ) contributes to detection, transduction and synaptic transfer of light stimuli in rod and cone photoreceptors. The function of Ca 2+ is highly compartmentalized. In the outer segment, Ca 2+ controls photoreceptor light adaptation by independently adjusting the gain of phototransduction at several stages in the transduction chain. In the inner segment and synaptic terminal, Ca 2+ regulates cells' metabolism, glutamate release, cytoskeletal dynamics, gene expression and cell death. We discuss the mechanisms of Ca 2+ entry, buffering, sequestration, release from internal stores and Ca 2+ extrusion from both outer and inner segments, showing that these two compartments have little in common with respect to Ca 2+ homeostasis. We also investigate the various roles played by Ca 2+ as an integrator of intracellular signaling pathways, and emphasize the central role played by Ca 2+ as a second messenger in neuromodulation of photoreceptor signaling by extracellular ligands such as dopamine, adenosine and somatostatin. Finally, we review the intimate link between dysfunction in photoreceptor Ca 2+ homeostasis and pathologies leading to retinal dysfunction and blindness. KeywordsRetina; Photoreceptor; Rod; Cone; Calcium; Plasma Membrane Calcium Atpase; Na-Ca Exchange; Calcium Store; Calcium Buffering; Calcium Channel; Calcium Extrusion; Ryanodine; Inner Segment; Dystrophy; Synaptic Transmission; Review INTRODUCTIONThe calcium ion (Ca 2+ ) is a major messenger for coordinating activity of eukaryote cells. Its extensive distribution and functioning as a control ion is common to a huge range of eukaryote cell types from animal, plant or fungal sources which diverged billions of years ago. The signaling potential of Ca 2+ is linked to the ability of cells to maintain a large concentration gradient between the cytosol (with basal Ca 2+ levels typically ~ 50 nM) and the extracellular media (with Ca 2+ ~ 1.5 mM). Because of this 10,000-fold difference in [Ca 2+ ]i between the cytosol and the extracellular space, Ca 2+ influx across the plasma membrane and Ca 2+ release from intracellular stores may produce large fluctuations of free cytosolic Ca 2+ (1). Another important feature of Ca 2+ homeostasis is that [Ca 2+ ]i elevations in the cell can be highly localized. We now know that the diffusion of Ca 2+ within the cytosol is much slower than that of other intracellular messengers (2,3). Ca 2+ is thus able to regulate a variety of different functions in different parts of the cell. Such selective action of Ca 2+ is facilitated by Ca 2+ -binding proteins which are often localized to specific sites mediating individual functions (4). To understand Ca 2+ signaling, it is therefore essential to map the spatial distribution of Ca 2+ effector proteins such as Ca 2+ channels, Ca 2+ pumps, cytoplasmic buffers and intracellular Anatomically, primary sensory neurons are notable for their compartmentalization into input ...

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“…The light-sensitive conductance of rods is a cGMP-dependent conductance (Fesenko, Kolesnikov & Lynbarsky, 1985;Yau & Nakatani, 1985;Zimmerman et al, 1985;Matthews, 1987), which can pass a current of Ca 2+ (Capovilla et al, 1983;Yau & Nakatani, 1984b;Hodgkin et al, 1985). The second pathway for Ca 2+ transport is Na-Ca exchange (Schnetkamp, 1980;Yau & Nakatani, 1984b;Schnetkamp, 1986;Hodgkin, McNaughton & Nunn, 1987;Schnetkamp & Bownds, 1987). Both pathways have a considerable capacity and can change total intracellular Ca 2 § by as much as 0.1 (amphibian rods) -0.5 (bovine rods) mM/sec.…”

Section: Introductionmentioning

confidence: 99%

Silver ions induce a rapid Ca2+ release from isolated intact bovine rod outer segments by a cooperative mechanism

Schnetkamp

Szerencsei

1989

J. Membrain Biol.

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Micromolar concentrations of silver ion activate large Ca2+ fluxes across the plasma membrane of intact rod outer segments isolated from bovine retinas (intact ROS). The rate of Ag+-induced Ca2+ efflux from intact ROS depended on the Ag+ concentration in a sigmoidal manner suggesting a cooperative mechanism with a Hill coefficient between 2 and 3. At a concentration of 50 microM Ag+ the rate of Ca2+ efflux was 7 x 10(6) Ca2+/outer segment/sec; this represents a change in total intracellular Ca2+ by 0.7 mM/outer segment/sec. Addition of the nonselective ionophore gramicidin in the absence of external alkali cations greatly reduced the Ag+-induced Ca2+ efflux from intact ROS, apparently by enabling internal alkali cations to leak out. Adding back alkali cations to the external medium restored Ag+-induced Ca2+ efflux when gramicidin was present. In the presence of gramicidin, Ag+-induced Ca2+ efflux from intact ROS was blocked by 50 microM tetracaine or L-cis diltiazem, whereas without gramicidin both blockers were ineffective. Both L-cis diltiazem and tetracaine are blockers of one kinetic component of cGMP-induced Ca2+ flux across ROS disk membranes. The ion selectivity of the Ag+-induced pathway proved to be broad with little discrimination between the alkali cations Li+, Na+, K+, and Cs+ or between Ca2+ and Mg2+. The properties of the Ag+-induced pathway(s) suggest that it may reflect the cGMP-dependent conductance opened in the absence of cGMP by silver ions.

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Na+- and cGMP-induced Ca2+ fluxes in frog rod photoreceptors.

Cited by 33 publications

References 37 publications

Slow inward tail currents in rabbit cardiac cells.

Slow inward tail currents in rabbit cardiac cells.

Calcium regulation in photoreceptors

Silver ions induce a rapid Ca2+ release from isolated intact bovine rod outer segments by a cooperative mechanism

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