Two mechanisms of quantized calcium release in skeletal muscle

Klein, Michael G.; Cheng, Heping; Santana, Luis Fernando; Jiang, Yuhua; Lederer, W. J.; Schneider, Martin F.

doi:10.1038/379455a0

Cited by 285 publications

(348 citation statements)

References 31 publications

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“…The marked disparity between the time course of the Ca 2ϩ rise and the duration of an action potential further strengthens the argument that most of the Ca 2ϩ rise comes from release from internal stores and not from influx via voltage-gated Ca 2ϩ channels. The time scale of 10 -15 msec is similar to that observed for amplification mechanisms in smooth muscle, cardiac muscle, and skeletal muscle (Cannell et al, 1995;Nelson et al, 1995;Klein et al, 1996). Figure 3A shows a spatial analysis of the Ca 2ϩ release sites in a surface plot of the fluorescence intensity (z-axis) along a line across the soma (x-axis) as a function of time after the field pulse ( y-axis).…”

Section: Rapid Kinetics and Spatial Analysis Of Intracellular Ca 2؉ Amentioning

confidence: 87%

“…Similar volume-to-surface limitations also exist for cardiac and skeletal muscle, in which intracellular Ca 2ϩ channels are opened by Ca 2ϩ -induced ryanodine receptor opening (Cannell et al, 1995) and by an electromechanical coupling between the dihydropyridine receptor and the ryanodine receptor (Klein et al, 1996). Thus, internal somatic Ca 2ϩ amplification can be used to amplify a short action potential-induced Ca 2ϩ influx at the plasma membrane into a functionally significant Ca 2ϩ response without requiring a large density of voltage-gated Ca 2ϩ channels in the soma.…”

Section: Discussionmentioning

confidence: 99%

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Control of Action Potential-Induced Ca²⁺Signaling in the Soma of Hippocampal Neurons by Ca²⁺Release from Intracellular Stores

Jacobs

Meyer

1997

J. Neurosci.

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Stimulus-induced increases in neuronal CaHere we used fluorescent Ca 2ϩ measurements in cultured hippocampal neurons and report that the amplitude of the somatic Ca 2ϩ increase triggered by field stimulation is independent of the extracellular Ca 2ϩ concentration as long as the concentration is greater than 50 M. Furthermore, significantly more La 3ϩ has to be added extracellularly for blocking Ca 2ϩ responses, as predicted from the reported La 3ϩ dependence of voltage-gated Ca 2ϩ channels. These measurements suggest that field stimulation-induced somatic Ca 2ϩ responses in hippocampal neurons are largely attributable to Ca 2ϩ release from intracellular stores. Only a small number of Ca 2ϩ ions have to enter across the plasma membrane for this intracellular Ca 2ϩ amplification process to occur. Rapid fluorescence-imaging measurements showed that the internal Ca 2ϩ amplification occurs over 10 -15 msec and linearly increases intracellular Ca 2ϩ concentrations for up to 40 action potentials. At a fixed number of field pulses, frequencies of 40 Hz were optimal for somatic Ca 2ϩ increases. Our studies suggest that the opening of intracellular Ca 2ϩ release channels plays a crucial part in shaping the action potential-induced neuronal Ca 2ϩ response.

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Section: Rapid Kinetics and Spatial Analysis Of Intracellular Ca 2؉ Amentioning

confidence: 87%

Section: Discussionmentioning

confidence: 99%

Control of Action Potential-Induced Ca²⁺Signaling in the Soma of Hippocampal Neurons by Ca²⁺Release from Intracellular Stores

Jacobs

Meyer

1997

J. Neurosci.

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“…The most likely possibility is that RyR3 are activated by the wave of Ca 2ϩ resulting from opening of RyR1 (7,34,36,37). Indeed a ''dual control'' of Ca release and an effect of RyR3 presence on the size of calcium sparks have been demonstrated (38,39). It should be noted that in RyR1-only muscles, half of the RyR1 may also be activated indirectly (9,32).…”

Section: Discussionmentioning

confidence: 99%

Type 3 ryanodine receptors of skeletal muscle are segregated in a parajunctional position

Felder

Franzini‐Armstrong

2002

Proc. Natl. Acad. Sci. U.S.A.

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A key event in skeletal muscle activation is the rapid release of Ca 2؉ from the sarcoplasmic reticulum (SR), the Ca 2؉ storage organelle in the muscle cell. The surface membrane͞transverse tubules and the SR form functional units (calcium release units containing one or two couplons or junctions), where the voltage-sensing dihydropyridine receptor of the surface membrane interacts with the SR Ca 2؉ release channel [ryanodine receptor (RyR)] and depolarization of the cell membrane is converted into Ca 2؉ release from the SR. Although RyR1 is the most important isoform in skeletal muscle, some muscles also express high levels of RyR3, an isoform with a wide tissue distribution. The cytoplasmic domains of RyRs are visible in the electron microscope as periodically disposed feet. We find that, in muscles containing only RyR1, feet are exclusively located over the junctional SR surface facing the surface membrane͞transverse tubule. In muscles containing RyR1 as well as RyR3, additional feet are located in lateral parajunctional regions immediately adjacent to junctional SR. Biochemical content of RyR3 and content of parajunctional feet are highly correlated in different muscles and the disposition of parajunctional versus junctional feet are notably different. On the basis of these two observations, we postulate that RyR3s are restricted to the parajunctional region, and thus their activation must be indirect and derivative during excitation-contraction coupling.

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“…Recent investigations have shown that localized and spontaneous intracellular calcium release events (i.e., calcium sparks) also arise from calcium release through ryanodine receptor channels in skeletal, cardiac, and smooth muscle cells (14)(15)(16)(17)(18)(19)(20). In porcine ASM cells, earlier studies revealed occurrence of calcium sparks that were grouped and coupled across adjacent regions of the cell (16).…”

Section: Spontaneous Calcium Release Events In Airway Smooth Muscle Cmentioning

confidence: 99%

Calcium Signaling in Airway Smooth Muscle

Jude¹,

Wylam²,

Walseth³

et al. 2008

Proceedings of the American Thoracic Society

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Contractility of airway smooth muscle requires elevation of intracellular calcium concentration. Under resting conditions, airway smooth muscle cells maintain a relatively low intracellular calcium concentration, and activation of the surface receptors by contractile agonists results in an elevation of intracellular calcium, culminating in contraction of the cell. The pattern of elevation of intracellular calcium brought about by agonists is a dynamic process and involves the coordinated activities of ion channels located in the plasma membrane and the sarcoplasmic reticulum. Among the signaling molecules involved in this dynamic calcium regulation in airway smooth muscle cells are inositol 1,4,5-trisphosphate and cyclic ADPribose, which mobilize calcium from the sarcoplasmic reticulum by acting via the inositol 1,4,5-trisphosphate and ryanodine receptors, respectively. In addition, calcium influx from the extracellular space is critical for the repletion of the intracellular calcium stores during activation of the cells by agonists. Calcium influx can occur via voltage-and receptor-gated channels in the plasma membrane, as well as by influx that is triggered by depletion of the intracellular stores (i.e., store-operated calcium entry mechanism). Transient receptor potential proteins appear to mediate the calcium influx via receptor-and store-operated channels. Recent studies have shown that proinflammatory cytokines regulate the expression and activity of the pathways involved in intracellular calcium regulation, thereby contributing to airway smooth muscle cell hyperresponsiveness. In this review, we will discuss the specific roles of cyclic ADP-ribose/ryanodine receptor channels and transient receptor potential channels in the regulation of intracellular calcium in airway smooth muscle cells. DYNAMIC INTRACELLULAR CALCIUM REGULATION IN AIRWAY SMOOTH MUSCLE CELLSExposure of airway smooth muscle (ASM) cells to contractile agonists results in a biphasic elevation of intracellular calcium concentration ([Ca 21 ] i ) that is characterized by an initial rapid and transient rise in calcium, followed by a decline to a lower, sustained steady-state concentration above the basal level (1-3). This biphasic [Ca 21 ] i response results from calcium influx from the extracellular space and release of calcium from the intracellular stores (i.e., the sarcoplasmic reticulum [SR]). Earlier studies have attributed the initial rapid and transient phase of the [Ca 21 ] i response to release from the SR, while the sustained phase of the response was thought to be due to influx from the extracellular space (2-6). Recent investigations using the improved temporal and spatial resolution features of real-time confocal microscopy have shed light on the dynamics of the [Ca 21 ] i response in ASM cells. These studies have shown that the biphasic [Ca 21 ] i response of ASM cells elicited by contractile agonists in reality consists of propagating regenerative calcium oscillations that originate at a location within a cell and propagate...

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Two mechanisms of quantized calcium release in skeletal muscle

Cited by 285 publications

References 31 publications

Control of Action Potential-Induced Ca²⁺Signaling in the Soma of Hippocampal Neurons by Ca²⁺Release from Intracellular Stores

Control of Action Potential-Induced Ca²⁺Signaling in the Soma of Hippocampal Neurons by Ca²⁺Release from Intracellular Stores

Type 3 ryanodine receptors of skeletal muscle are segregated in a parajunctional position

Calcium Signaling in Airway Smooth Muscle

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Two mechanisms of quantized calcium release in skeletal muscle

Cited by 285 publications

References 31 publications

Control of Action Potential-Induced Ca2+Signaling in the Soma of Hippocampal Neurons by Ca2+Release from Intracellular Stores

Control of Action Potential-Induced Ca2+Signaling in the Soma of Hippocampal Neurons by Ca2+Release from Intracellular Stores

Type 3 ryanodine receptors of skeletal muscle are segregated in a parajunctional position

Calcium Signaling in Airway Smooth Muscle

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Control of Action Potential-Induced Ca²⁺Signaling in the Soma of Hippocampal Neurons by Ca²⁺Release from Intracellular Stores

Control of Action Potential-Induced Ca²⁺Signaling in the Soma of Hippocampal Neurons by Ca²⁺Release from Intracellular Stores