Inositol 1,4,5-trisphosphate induced calcium waves

2008 ◽  
pp. 164-190 ◽  
Author(s):  
M. Falcke
Keyword(s):  
Calcium Waves ◽  
Inositol 1,4,5 Trisphosphate

The Sarcoplasmic Reticulum, Ca2+ Trapping, and Wave Mechanisms in Smooth Muscle

Physiology ◽  
2004 ◽  
Vol 19 (3) ◽  
pp. 138-147 ◽  
Author(s):  
John G. McCarron ◽  
Karen N. Bradley ◽  
Debbi MacMillan ◽  
Susan Chalmers ◽  
Thomas C. Muir
Keyword(s):  
Wave Propagation ◽  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Calcium Waves ◽  
Inositol 1,4,5 Trisphosphate

The sarcoplasmic reticulum (SR) and apposed regions of the sarcolemma passively trap Ca2+ entering the cell to limit the rise in cytoplasmic Ca2+ concentration without SR pump involvement. When “leaky” the SR facilitates Ca2+ entry to the cytoplasm. SR Ca2+ release via inositol 1,4,5-trisphosphate receptors (IP3Rs) propagates as calcium waves; IP3Rs alone account for wave propagation.

scholarly journals Voltage-gated Ca2+channel activity modulates smooth muscle cell calcium waves in hamster cremaster arterioles

2018 ◽  
Vol 315 (4) ◽  
pp. H871-H878 ◽  
Author(s):  
William F. Jackson ◽  
Erika M. Boerman
Keyword(s):  
Smooth Muscle ◽  
Channel Blocker ◽  
Muscle Tone ◽  
Myogenic Tone ◽  
Calcium Waves ◽  
Cremaster Muscle ◽  
Channel Activity ◽  
Voltage Gated ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

Cremaster muscle arteriolar smooth muscle cells (SMCs) display inositol 1,4,5-trisphosphate receptor-dependent Ca2+waves that contribute to global myoplasmic Ca2+concentration and myogenic tone. However, the contribution made by voltage-gated Ca2+channels (VGCCs) to arteriolar SMC Ca2+waves is unknown. We tested the hypothesis that VGCC activity modulates SMC Ca2+waves in pressurized (80 cmH2O/59 mmHg, 34°C) hamster cremaster muscle arterioles loaded with Fluo-4 and imaged by confocal microscopy. Removal of extracellular Ca2+dilated arterioles (32 ± 3 to 45 ± 3 μm, n = 15, P < 0.05) and inhibited the occurrence, amplitude, and frequency of Ca2+waves ( n = 15, P < 0.05), indicating dependence of Ca2+waves on Ca2+influx. Blockade of VGCCs with nifedipine (1 μM) or diltiazem (10 μM) or deactivation of VGCCs by hyperpolarization of smooth muscle with the K+channel agonist cromakalim (10 μM) produced similar inhibition of Ca2+waves ( P < 0.05). Conversely, depolarization of SMCs with the K+channel blocker tetraethylammonium (1 mM) constricted arterioles from 26 ± 3 to 14 ± 2 μm ( n = 11, P < 0.05) and increased wave occurrence (9 ± 3 to 16 ± 3 waves/SMC), amplitude (1.6 ± 0.07 to 1.9 ± 0.1), and frequency (0.5 ± 0.1 to 0.9 ± 0.2 Hz, n = 10, P < 0.05), effects that were blocked by nifedipine (1 μM, P < 0.05). Similarly, the VGCC agonist Bay K8644 (5 nM) constricted arterioles from 14 ± 1 to 8 ± 1 μm and increased wave occurrence (3 ± 1 to 10 ± 1 waves/SMC) and frequency (0.2 ± 0.1 to 0.6 ± 0.1 Hz, n = 6, P < 0.05), effects that were unaltered by ryanodine (50 μM, n = 6, P > 0.05). These data support the hypothesis that Ca2+waves in arteriolar SMCs depend, in part, on the activity of VGCCs.NEW & NOTEWORTHY Arterioles that control blood flow to and within skeletal muscle depend on Ca2+influx through voltage-gated Ca2+channels and release of Ca2+from internal stores through inositol 1,4,5-trisphosphate receptors in the form of Ca2+waves to maintain pressure-induced smooth muscle tone.

Mechanism of ACh-induced asynchronous calcium waves and tonic contraction in porcine tracheal muscle bundle

2006 ◽  
Vol 290 (3) ◽  
pp. L459-L469 ◽  
Author(s):  
Jiazhen M. Dai ◽  
Kuo-Hsing Kuo ◽  
Joyce M. Leo ◽  
Cornelis van Breemen ◽  
Cheng-Han Lee
Keyword(s):  
Cyclopiazonic Acid ◽  
Tonic Contraction ◽  
Calcium Waves ◽  
Muscle Bundle ◽  
Voltage Gated ◽  
Contraction Coupling ◽  
Reverse Mode ◽  
Plasmic Reticulum ◽  
Inositol 1,4,5 Trisphosphate ◽  
Stimulation Of

Stimulation of the tracheal muscle bundle by acetylcholine (ACh) results in the generation of asynchronous repetitive Ca2+ waves (ACW) in intact tracheal smooth muscle (TSM) cells. We showed previously that ACW underlie cholinergic excitation-contraction coupling in porcine TSM and that Ca2+ entry through the L-type voltage-gated Ca2+ channel (VGCC) contributes partially to maintenance of the ACW. However, the mechanism of the ACW remains undefined. In this study, we pharmacologically characterized the mechanism of ACh-induced ACW in the intact porcine tracheal muscle bundle. We found that inhibition of receptor-operated channels/store-operated channels (ROC/SOC) by SKF-96365 completely abolished the nifedipine-insensitive component of ACh-mediated ACW and tonic contraction. Blockade of Na+/Ca2+ exchange with KB-R7943 or 2′,4′-dichlorobenzamil or removal of extracellular Na+ resulted in nearly complete inhibition of the nifedipine-insensitive component of ACh-mediated ACW and tonic contraction. Inhibition of the sarco(endo)plasmic reticulum Ca2+-ATPase by cyclopiazonic acid abolished the ongoing ACW. Application of 2-aminoethoxydiphenyl borate (2-APB) or xestospongin C to inhibit the inositol 1,4,5-trisphosphate-sensitive sarcoplasmic reticulum (SR) Ca2+ release channels produced no effect on ACh-mediated ACW and tonic contraction. However, pretreatment with caffeine or ryanodine inhibited ACh-induced ACW. Furthermore, application of procaine or tetracaine prevented the generation and abolished the ongoing ACh-mediated ACW and tonic contraction. Collectively, these results indicate that the ACh-stimulated ACW in porcine TSM are produced by repetitive cycles of Ca2+ release from SR through 2-APB- and xestospongin C-insensitive Ca2+ release channels, and plasmalemmal Ca2+ entry involving reverse-mode Na+/Ca2+ exchange, ROC/SOC, and L-type VGCC is required to refill the SR via SERCA to support the ongoing ACW.

scholarly journals Astrocyte networks and intercellular calcium propagation

2018 ◽  
Author(s):  
Jules Lallouette ◽  
Maurizio De Pittà ◽  
Hugues Berry
Keyword(s):  
General Framework ◽  
Brain Area ◽  
Second Messengers ◽  
Morphological Diversity ◽  
Calcium Waves ◽  
Gap Junction Channels ◽  
Intracellular Signals ◽  
Inositol 1,4,5 Trisphosphate ◽  
Network Topologies ◽  
The Brain

AbstractAstrocytes organize in complex networks through connections by gap junction channels that are regulated by extra‐ and intracellular signals. Calcium signals generated in individual cells, can propagate across these networks in the form of intercellular calcium waves, mediated by diffusion of second messengers molecules such as inositol 1,4,5-trisphosphate. The mechanisms underpinning the large variety of spatiotemporal patterns of propagation of astrocytic calcium waves however remain a matter of investigation. In the last decade, awareness has grown on the morphological diversity of astrocytes as well as their connections in networks, which seem dependent on the brain area, developmental stage, and the ultrastructure of the associated neuropile. It is speculated that this diversity underpins an equal functional variety but the current experimental techniques are limited in supporting this hypothesis because they do not allow to resolve the exact connectivity of astrocyte networks in the brain. With this aim we present a general framework to model intercellular calcium wave propagation in astrocyte networks and use it to specifically investigate how different network topologies could influence shape, frequency and propagation of these waves.

Calcium waves and oscillations driven by an intercellular gradient of inositol (1,4,5)-trisphosphate

1998 ◽  
Vol 72 (1-2) ◽  
pp. 101-109 ◽  
Author(s):  
James Sneyd ◽  
Matthew Wilkins ◽  
Andreja Strahonja ◽  
Michael J. Sanderson
Keyword(s):  
Calcium Waves ◽  
Inositol 1,4,5 Trisphosphate

A model for the propagation of intercellular calcium waves

1994 ◽  
Vol 266 (1) ◽  
pp. C293-C302 ◽  
Author(s):  
J. Sneyd ◽  
A. C. Charles ◽  
M. J. Sanderson
Keyword(s):  
Experimental Data ◽  
Gap Junctions ◽  
Cell Cultures ◽  
Calcium Waves ◽  
Airway Epithelial ◽  
Good Qualitative Agreement ◽  
Inositol 1,4,5 Trisphosphate ◽  
A Cell ◽  
Glial Cell Cultures ◽  
Stimulation Of

In response to mechanical stimulation of a single cell, intercellular Ca2+ waves propagate through airway epithelial and glial cell cultures, providing a mechanism for intercellular communication. Experiments indicate that intercellular propagation of the Ca2+ wave is mediated by the movement of inositol 1,4,5-trisphosphate (IP3) through gap junctions. To explore the validity of this hypothesis, we have constructed and solved a system of partial differential equations that models the Ca2+ changes induced by the movement of IP3 between cells. The model is in good qualitative agreement with experimental data, including the behavior of the wave in the absence of extracellular Ca2+, the shape of the subsequent asynchronous Ca2+ oscillations, and the passage of a wave through a cell exhibiting Ca2+ oscillations. However, the concentration of IP3 that is required in each cell to propagate the wave may not be achieved by passive diffusion of IP3 through gap junctions from the stimulated cell. We therefore suggest that Ca(2+)-independent regenerative production of IP3 might be necessary for the propagation of intercellular Ca2+ waves.

scholarly journals Radial Localization of Inositol 1,4,5-Trisphosphate–sensitive Ca2+ Release Sites in Xenopus Oocytes Resolved by Axial Confocal Linescan Imaging

1999 ◽  
Vol 113 (2) ◽  
pp. 199-213 ◽  
Author(s):  
Nick Callamaras ◽  
Ian Parker
Keyword(s):  
Xenopus Oocytes ◽  
Calcium Release ◽  
Calcium Influx ◽  
Calcium Waves ◽  
Radial Line ◽  
Calcium Dependent ◽  
Inositol 1,4,5 Trisphosphate ◽  
Radial Spread ◽  
Punctate Staining ◽  
Radial Organization

The radial localization and properties of elementary calcium release events (“puffs”) were studied in Xenopus oocytes using a confocal microscope equipped with a piezoelectric focussing unit to allow rapid (&gt;100 Hz) imaging of calcium signals along a radial line into the cell with a spatial resolution of &lt;0.7 μm. Weak photorelease of caged inositol 1,4,5-trisphosphate (InsP3) evoked puffs arising predominantly within a 6-μm thick band located within a few micrometers of the cell surface. Approximately 25% of puffs had a restricted radial spread, consistent with calcium release from a single site. Most puffs, however, exhibited a greater radial spread (3.25 μm), likely involving recruitment of radially neighboring release sites. Calcium waves evoked by just suprathreshold stimuli exhibited radial calcium distributions consistent with inward diffusion of calcium liberated at puff sites, whereas stronger flashes evoked strong, short-latency signals at depths inward from puff sites, indicating deep InsP3-sensitive stores activated at higher concentrations of InsP3. Immunolocalization of InsP3 receptors showed punctate staining throughout a region corresponding to the localization of puffs and subplasmalemmal endoplasmic reticulum. The radial organization of puff sites a few micrometers inward from the plasma membrane may have important consequences for activation of calcium-dependent ion channels and “capacitative” calcium influx. However, on the macroscopic (hundreds of micrometers) scale of global calcium waves, release can be considered to occur primarily within a thin, essentially two-dimensional subplasmalemmal shell.

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