scholarly journals Prolonged calcium influx after termination of light-induced calcium release in invertebrate photoreceptors

2009 ◽  
Vol 134 (3) ◽  
pp. 177-189 ◽  
Author(s):  
Maria del Pilar Gomez ◽  
Enrico Nasi
Keyword(s):  
Calcium Release ◽  
Calcium Influx ◽  
Alternative Pathway ◽  
Membrane Conductance ◽  
Receptor Potential ◽  
Cytosolic Calcium ◽  
Slow Inward Current ◽  
Alternative Mechanism ◽  
Large Size ◽  
Gradual Development

In microvillar photoreceptors, light stimulates the phospholipase C cascade and triggers an elevation of cytosolic Ca2+ that is essential for the regulation of both visual excitation and sensory adaptation. In some organisms, influx through light-activated ion channels contributes to the Ca2+ increase. In contrast, in other species, such as Lima, Ca2+ is initially only released from an intracellular pool, as the light-sensitive conductance is negligibly permeable to calcium ions. As a consequence, coping with sustained stimulation poses a challenge, requiring an alternative pathway for further calcium mobilization. We observed that after bright or prolonged illumination, the receptor potential of Lima photoreceptors is followed by the gradual development of an after-depolarization that decays in 1–4 minutes. Under voltage clamp, a graded, slow inward current (Islow) can be reproducibly elicited by flashes that saturate the photocurrent, and can reach a peak amplitude in excess of 200 pA. Islow obtains after replacing extracellular Na+ with Li+, guanidinium, or N-methyl-d-glucamine, indicating that it does not reflect the activation of an electrogenic Na/Ca exchange mechanism. An increase in membrane conductance accompanies the slow current. Islow is impervious to anion replacements and can be measured with extracellular Ca2+ as the sole permeant species; Ba can substitute for Ca2+ but Mg2+ cannot. A persistent Ca2+ elevation parallels Islow, when no further internal release takes place. Thus, this slow current could contribute to sustained Ca2+ mobilization and the concomitant regulation of the phototransduction machinery. Although reminiscent of the classical store depletion–operated calcium influx described in other cells, Islow appears to diverge in some significant aspects, such as its large size and insensitivity to SKF96365 and lanthanum; therefore, it may reflect an alternative mechanism for prolonged increase of cytosolic calcium in photoreceptors.

scholarly journals The Role of Ca2+-NFATc1 Signaling and Its Modulation on Osteoclastogenesis

2020 ◽  
Vol 21 (10) ◽  
pp. 3646
Author(s):  
Jung Yun Kang ◽  
Namju Kang ◽  
Yu-Mi Yang ◽  
Jeong Hee Hong ◽  
Dong Min Shin
Keyword(s):  
Bone Loss ◽  
Calcium Signaling ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Osteoclast Differentiation ◽  
Receptor Potential ◽  
Cytosolic Calcium ◽  
Transient Receptor Potential Channels ◽  
Potential Channels ◽  
Transient Receptor

The increasing of intracellular calcium concentration is a fundamental process for mediating osteoclastogenesis, which is involved in osteoclastic bone resorption. Cytosolic calcium binds to calmodulin and subsequently activates calcineurin, leading to NFATc1 activation, a master transcription factor required for osteoclast differentiation. Targeting the various activation processes in osteoclastogenesis provides various therapeutic strategies for bone loss. Diverse compounds that modulate calcium signaling have been applied to regulate osteoclast differentiation and, subsequently, attenuate bone loss. Thus, in this review, we summarized the modulation of the NFATc1 pathway through various compounds that regulate calcium signaling and the calcium influx machinery. Furthermore, we addressed the involvement of transient receptor potential channels in osteoclastogenesis.

scholarly journals Sodium/Calcium Exchangers Selectively Regulate Calcium Signaling in Mouse Taste Receptor Cells

2010 ◽  
Vol 104 (1) ◽  
pp. 529-538 ◽  
Author(s):  
Steven A. Szebenyi ◽  
Agnieszka I. Laskowski ◽  
Kathryn F. Medler
Keyword(s):  
Calcium Release ◽  
Calcium Influx ◽  
Taste Receptor ◽  
Physiological Role ◽  
Cytosolic Calcium ◽  
Calcium Signals ◽  
Sodium Calcium ◽  
Signaling Mechanisms ◽  
Taste Cells ◽  
Mouse Taste

Taste cells use multiple signaling mechanisms to generate appropriate cellular responses to discrete taste stimuli. Some taste stimuli activate G protein coupled receptors (GPCRs) that cause calcium release from intracellular stores while other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). While the signaling mechanisms that initiate calcium signals have been described in taste cells, the calcium clearance mechanisms (CCMs) that contribute to the termination of these signals have not been identified. In this study, we used calcium imaging to define the role of sodium-calcium exchangers (NCXs) in the termination of evoked calcium responses. We found that NCXs regulate the calcium signals that rely on calcium influx at the plasma membrane but do not significantly contribute to the calcium signals that depend on calcium release from internal stores. Our data indicate that this selective regulation of calcium signals by NCXs is due primarily to their location in the cell rather than to the differences in cytosolic calcium loads. This is the first report to define the physiological role for any of the CCMs utilized by taste cells to regulate their evoked calcium responses.

scholarly journals PKCα mediates acetylcholine-induced activation of TRPV4-dependent calcium influx in endothelial cells

2011 ◽  
Vol 301 (3) ◽  
pp. H757-H765 ◽  
Author(s):  
Ravi K. Adapala ◽  
Phani K. Talasila ◽  
Ian N. Bratz ◽  
David X. Zhang ◽  
Makoto Suzuki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Specific Inhibitor ◽  
Receptor Potential ◽  
Cyclic Stretch ◽  
Mesenteric Arteries ◽  
Transient Receptor Potential Vanilloid

Transient receptor potential vanilloid channel 4 (TRPV4) is a polymodally activated nonselective cationic channel implicated in the regulation of vasodilation and hypertension. We and others have recently shown that cyclic stretch and shear stress activate TRPV4-mediated calcium influx in endothelial cells (EC). In addition to the mechanical forces, acetylcholine (ACh) was shown to activate TRPV4-mediated calcium influx in endothelial cells, which is important for nitric oxide-dependent vasodilation. However, the molecular mechanism through which ACh activates TRPV4 is not known. Here, we show that ACh-induced calcium influx and endothelial nitric oxide synthase (eNOS) phosphorylation but not calcium release from intracellular stores is inhibited by a specific TRPV4 antagonist, AB-159908. Importantly, activation of store-operated calcium influx was not altered in the TRPV4 null EC, suggesting that TRPV4-dependent calcium influx is mediated through a receptor-operated pathway. Furthermore, we found that ACh treatment activated protein kinase C (PKC) α, and inhibition of PKCα activity by the specific inhibitor Go-6976, or expression of a kinase-dead mutant of PKCα but not PKCε or downregulation of PKCα expression by chronic 12- O-tetradecanoylphorbol-13-acetate treatment, completely abolished ACh-induced calcium influx. Finally, we found that ACh-induced vasodilation was inhibited by the PKCα inhibitor Go-6976 in small mesenteric arteries from wild-type mice, but not in TRPV4 null mice. Taken together, these findings demonstrate, for the first time, that a specific isoform of PKC, PKCα, mediates agonist-induced receptor-mediated TRPV4 activation in endothelial cells.

Ionomycin-stimulated phasic myometrial contractions

1995 ◽  
Vol 269 (4) ◽  
pp. E779-E785
Author(s):  
M. Phillippe ◽  
E. M. Chien ◽  
M. Freij ◽  
T. Saunders
Keyword(s):  
Phospholipase C ◽  
Calcium Release ◽  
Calcium Influx ◽  
Inositol Phosphate ◽  
Calcium Ionophore ◽  
Cytosolic Calcium ◽  
Calcium Oscillations ◽  
Production Studies ◽  
Inositol Phosphate Production

Ionomycin, a calcium ionophore, facilitates the sustained entry of extracellular calcium; however, in myometrial tissue it stimulates phasic contractions. This study sought to define further this unanticipated effect of ionomycin and to begin to explore the possible mechanism(s) involved. Utilizing rat uterine strips, in vitro isometric contraction studies were performed to determine the effects of ionomycin with and without membrane-permeant inhibitors of cytosolic calcium oscillations. To determine the effects of ionomycin on phospholipase C, qualitative inositol phosphate production studies were performed. The in vitro contraction studies confirmed that ionomycin-stimulated phasic myometrial contractions were potentially dependent on stimulation of phospholipase C, calcium-induced calcium release, and additional calcium influx through dihydropyridine-sensitive membrane calcium channels. The inositol phosphate production studies confirmed that ionomycin stimulated phospholipase C in a dose-related fashion to levels comparable to oxytocin. In summary, these observations have confirmed the ability of ionomycin to generate dose-related phasic myometrial contractions through mechanisms potentially involving the phosphatidylinositol-signaling pathway.

scholarly journals Mitochondrial Calcium Buffering Contributes to the Maintenance of Basal Calcium Levels in Mouse Taste Cells

2008 ◽  
Vol 100 (4) ◽  
pp. 2177-2191 ◽  
Author(s):  
Kyle Hacker ◽  
Kathryn F. Medler
Keyword(s):  
Signaling Pathways ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Taste Receptor ◽  
Cell Types ◽  
Cytosolic Calcium ◽  
Mitochondrial Calcium ◽  
Calcium Buffering ◽  
Taste Cells

Taste stimuli are detected by taste receptor cells present in the oral cavity using diverse signaling pathways. Some taste stimuli are detected by G protein–coupled receptors (GPCRs) that cause calcium release from intracellular stores, whereas other stimuli depolarize taste cells to cause calcium influx through voltage-gated calcium channels (VGCCs). Although taste cells use two distinct mechanisms to transmit taste signals, increases in cytosolic calcium are critical for normal responses in both pathways. This creates a need to tightly control intracellular calcium levels in all transducing taste cells. To date, however, the mechanisms used by taste cells to regulate cytosolic calcium levels have not been identified. Studies in other cell types have shown that mitochondria can be important calcium buffers, even during small changes in calcium loads. In this study, we used calcium imaging to characterize the role of mitochondria in buffering calcium levels in taste cells. We discovered that mitochondria make important contributions to the maintenance of resting calcium levels in taste cells by routinely buffering a constitutive calcium influx across the plasma membrane. This is unusual because in other cell types, mitochondrial calcium buffering primarily affects large evoked calcium responses. We also found that the amount of calcium that is buffered by mitochondria varies with the signaling pathways used by the taste cells. A transient receptor potential (TRP) channel, likely TRPV1 or a taste variant of TRPV1, contributes to the constitutive calcium influx.

scholarly journals Calcium signaling mediates mechanotransduction at the multicellular stage of Dictyostelium discoideum

2021 ◽  
Author(s):  
Hidenori Hashimura ◽  
Yusuke V. Morimoto ◽  
Yusei Hirayama ◽  
Masahiro Ueda
Keyword(s):  
Calcium Signaling ◽  
Dictyostelium Discoideum ◽  
Molecular Mechanisms ◽  
Calcium Release ◽  
Calcium Influx ◽  
Cytosolic Calcium ◽  
Calcium Signal ◽  
Mechanical Stimuli ◽  
Ip3 Receptor ◽  
Cellular Functions

Calcium acts as a second messenger and regulates cellular functions, including cell motility. In Dictyostelium discoideum, the cytosolic calcium level oscillates synchronously, and calcium signal waves propagate in the cell population during the early stages of development, including aggregation. At the unicellular phase, the calcium response through Piezo channels also functions in mechanosensing. However, calcium signaling dynamics during multicellular morphogenesis is still unclear. Here, live-imaging of cytosolic calcium levels revealed that calcium wave propagation, depending on cAMP relay, temporarily disappeared at the onset of multicellular body formation. Alternatively, the occasional burst of calcium signals and their propagation were observed in both anterior and posterior regions of migrating multicellular bodies. Calcium signaling in multicellular bodies occurred in response to mechanical stimulation. Both pathways, calcium release from the endoplasmic reticulum via IP3 receptor and calcium influx from outside the cell, were involved in calcium waves induced by mechanical stimuli. These show that calcium signaling works on mechanosensing in both the unicellular and multicellular phases of Dictyostelium using different molecular mechanisms during development.

scholarly journals Calcium-induced calcium release in noradrenergic neurons of the locus coeruleus

2019 ◽  
Author(s):  
Hiroyuki Kawano ◽  
Sara B. Mitchell ◽  
Jin-Young Koh ◽  
Kirsty M. Goodman ◽  
N. Charles Harata
Keyword(s):  
Locus Coeruleus ◽  
Calcium Release ◽  
Reversal Potential ◽  
Outward Current ◽  
Membrane Conductance ◽  
Cytosolic Calcium ◽  
Equilibrium Potential ◽  
Calcium Stores ◽  
Patch Clamp Recording ◽  
Calcium Induced Calcium Release

ABSTRACTThe locus coeruleus (LC) is a nucleus within the brainstem that consists of norepinephrine-releasing neurons. It is involved in broad processes including autonomic regulation, and cognitive and emotional functions such as arousal, attention and anxiety. Understanding the mechanisms that control the excitability of LC neurons is important because they innervate widespread regions of the central nervous system. One of the key regulators is the cytosolic calcium concentration ([Ca2+]c), the increases in which can be amplified by calcium-induced calcium release (CICR) from the intracellular calcium stores. Although the electrical activities of LC neurons are regulated by changes in [Ca2+]c, the extent of CICR involvement in this regulation has remained unclear. Here we show that CICR hyperpolarizes acutely dissociated LC neurons of the rat brain and demonstrate the pathway whereby it does this. When CICR was activated by extracellular application of 10 mM caffeine, LC neurons were hyperpolarized in the current-clamp mode of the patch-clamp recording, and the majority of neurons showed an outward current in the voltage-clamp mode. This outward current was accompanied by an increase in membrane conductance, and its reversal potential was close to the K+ equilibrium potential, indicating that it is mediated by the opening of K+ channels. The outward current was generated in the absence of extracellular calcium and was blocked when the calcium stores were inhibited by applying ryanodine. Pharmacological experiments indicated that the outward current was mediated by Ca2+-activated K+ channels of the non-small conductance type. Finally, the application of caffeine led to an increase in the [Ca2+]c in these neurons, as visualized by fluorescence microscopy. These findings delineate a mechanism whereby CICR suppresses the electrical activity of LC neurons, and indicate that it could play a dynamic role in modulating the LC-mediated noradrenergic tone in the brain.

scholarly journals New Insights on the Role of TRP Channels in Calcium Signalling and Immunomodulation: Review of Pathways and Implications for Clinical Practice

2021 ◽  
Author(s):  
Saied Froghi ◽  
Charlotte R. Grant ◽  
Radhika Tandon ◽  
Alberto Quaglia ◽  
Brian Davidson ◽  
...  
Keyword(s):  
Immune System ◽  
Calcium Release ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Calcium Influx ◽  
Calcium Signalling ◽  
Chronic Fatigue ◽  
Diverse Range ◽  
Immune System Activation

AbstractCalcium is the most abundant mineral in the human body and is central to many physiological processes, including immune system activation and maintenance. Studies continue to reveal the intricacies of calcium signalling within the immune system. Perhaps the most well-understood mechanism of calcium influx into cells is store-operated calcium entry (SOCE), which occurs via calcium release-activated channels (CRACs). SOCE is central to the activation of immune system cells; however, more recent studies have demonstrated the crucial role of other calcium channels, including transient receptor potential (TRP) channels. In this review, we describe the expression and function of TRP channels within the immune system and outline associations with murine models of disease and human conditions. Therefore, highlighting the importance of TRP channels in disease and reviewing potential. The TRP channel family is significant, and its members have a continually growing number of cellular processes. Within the immune system, TRP channels are involved in a diverse range of functions including T and B cell receptor signalling and activation, antigen presentation by dendritic cells, neutrophil and macrophage bactericidal activity, and mast cell degranulation. Not surprisingly, these channels have been linked to many pathological conditions such as inflammatory bowel disease, chronic fatigue syndrome and myalgic encephalomyelitis, atherosclerosis, hypertension and atopy.

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

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