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Query: CAS:7440-70-2 (calcium)
 333,191 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ovarian oocytes of the prosobranch mollusc Patella vulgata and the pelecypod Ruditapes philippinarum are arrested during prophase of the first maturation division. Release from this blockade, which is revealed by germinal vesicle breakdown, drives these oocytes to a second arrest in metaphase I, at which time the oocytes become fertilizable. The respective roles of Ca2+ and H+ ion movements during this early step in meiosis reinitiation has not been fully established yet. In this work we reveal the presence of acidic vesicles and report that bafilomycin A1 and N,N'-dicyclohexylcarbodiimide, two inhibitors of the vacuolar-type H(+)-ATPase, applied to Ruditapes oocytes, produce a significant inhibition of their response to the natural neurohormone serotonin. Since sodium deprivation did not affect this response, this suggests that a v-type ATPase pump, possibly located in the membrane of these acidic vesicles, may play a subtle role in the cascade of events that releases oocytes from their prophase block. We then describe how 4-aminopyridine, a drug reputed to be a K+ channel antagonist, triggers both meiosis reinitiation and activation of Patella and Ruditapes oocytes. This agent acts as a weak base, its effect depending on external pH. Moreover, using the fluorescent probes BCECF and Fluo-3/AM, we observe that this drug both alkalinizes the endoplasm and promotes an intracellular Ca2+ surge. This dual effect may explain why Ruditapes oocytes no longer stop in metaphase under these conditions and behave like other bivalve species which are directly fertilizable at the germinal vesicle stage.
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PMID:4-aminopyridine acts as a weak base and a Ca2+ mobilizing agent in triggering oocyte meiosis reinitiation and activation in the Japanese clam Ruditapes philippinarum. 757 39

The molecular events associated with beta-amyloid-induced neuronal injury remain incompletely characterized. Using a substantia nigra/neuroblastoma hybrid cell line (MES 23.5) synthetic beta-amyloid 1-40 induced a time and dose-dependent apoptotic cell death which was characterized by cell shrinkage and fragmentation of DNA, and was inhibited by aurintricarboxylic acid (ATA), and cycloheximide (CHX). Following beta-amyloid 1-40 treatment, cyclic GMP, an index of NO synthesis, was increased in MES 23.5 cells. The NO scavenger hemoglobin, as well as the NO synthase inhibitors NG-monomethyl-L-arginine acetate (L-NMMA) and L-N5-(1-iminoethyl)ornithine hydrochloride (L-NI0) attenuated such increases. These same inhibitors and scavengers also significantly prevented cytotoxicity. beta-Amyloid also induced an early and transient increase in intracellular calcium as monitored with laser scanning confocal microscopy and Fluo-3 imaging. These induced calcium transients could be significantly blocked by the N-methyl-D-aspartic acid (NMDA) receptor antagonist MK-801. Pretreatment with MK-801 or removal of extracellular Ca2+ also reduced beta-amyloid-induced NO production and neurotoxicity. Furthermore, beta-amyloid neurotoxicity was greatly enhanced in the absence of Mg2+ or in the presence of glutamate or NMDA. These data suggest that beta-amyloid can lead to apoptotic cell death through a NO mediated process possibly triggered by Ca2+ entry through activated NMDA-gated channels.
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PMID:Cell death induced by beta-amyloid 1-40 in MES 23.5 hybrid clone: the role of nitric oxide and NMDA-gated channel activation leading to apoptosis. 758 71

Cultured hind limb skeletal muscle cells from newborn rats were used to study the effect of caffeine and tetracaine upon intracellular Ca2+ release under voltage or current clamp conditions. Free [Ca2+]i was measured using the fluorescent calcium-sensitive dye Fluo-3. A field containing one or several myotubes was observed with a video camera and image analysis of fluorescence changes was performed. Addition of 100-500 microM tetracaine to the external saline elicited strong fluorescence responses in non-clamped cells, but significantly lower responses in cells clamped at -90 mV. At the same time, tetracaine inhibited voltage induced calcium release. Voltage and tetracaine modulation over the action of caffeine (500 microM) was also observed. Pretreatment of cells with 10 microM nifedipine abolished the caffeine induced fluorescence response in non-clamped cells. These findings suggest that, in cultured muscle cells, calcium release through the caffeine and tetracaine sensitive pathways is controlled by both membrane potential and the dihydropyridine receptor.
Cell Calcium 1995 Aug
PMID:Voltage control of calcium transients elicited by caffeine and tetracaine in cultured rat muscle cells. 758 91

Dual-excitation confocal laser scanning microscopy (CLSM) was used to image the pH-indicator, BCECF, iontophoretically microinjected into stomatal guard cells of Vicia faba during challenge with peptides derived from hydrophilic domains of the maize auxin-binding protein. Only the peptide corresponding to the C-terminal end (Pz151-163) caused significant changes in cytosolic pH, stimulating rapid alkalinisation of 0.4 +/- 0.1 pH units. Cytosolic pH was clamped using the permeant weak acid, butyrate, and this treatment buffered the peptide evoked alkalinisation. In concert with the electrical events monitored at the plasma membrane using whole-cell voltage clamp, this provides strong evidence for a role of [H+] as a signal intermediate in the guard cell transduction network. In preliminary experiments using single-wavelength imaging of the calcium-indicator, Fluo-3, Pz151-163 also stimulated rapid, reversible increases in cytosolic calcium, whilst two other peptides tested had no effect.
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PMID:Peptides derived from the auxin binding protein elevate Ca2+ and pH in stomatal guard cells of Vicia faba: a confocal fluorescence ratio imaging study. 759 45

Simultaneous Ca2+ measurements in the cytosol and intracellular stores (IS) of rat hepatocytes were performed using two Ca(2+)-sensitive probes (Fluo-3 and Mag-fura-2), and combined whole-cell patch clamp and fluorescence microscopy. A steady-state Ca2+ concentration of approximately 630 microM was estimated in the IS. alpha 1-Adrenergic stimulation induced periodic elevations of cytosolic Ca2+ and parallel synchronized transient declines in the IS. Subsequent application of the intracellular Ca(2+)-pump inhibitor thapsigargin resulted in a release of Ca2+ from the IS to reach a level of Ca2+ depletion much lower than the lowest transient decline observed during the oscillations.
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PMID:Simultaneous measurements of Ca2+ in the intracellular stores and the cytosol of hepatocytes during hormone-induced Ca2+ oscillations. 761 74

The purpose of this study was to characterize the effect of various shear conditions on endothelial cell intracellular calcium ([Ca2+]i). Bovine aortic endothelial cells (BAEC) were loaded with Fluo-3 and exposed to flow in a parallel plate flow chamber designed for confocal microscopy. The flow medium was medium 199 (M-199), which was prepared with and without adenosine triphosphate (ATP). In the presence of ATP, initiation of flow at a shear stress of 2.5 dyn/cm2 evoked a strong, sustained elevation of [Ca2+]i that gradually returned to baseline levels over 10 to 15 min. By contrast, in the absence of ATP, initiation of flow at 2.5 dyn/cm2 produced only transient increases in [Ca2+]i in a small proportion of the cells. As shear rate was increased from 2.5 to 15 dyn/cm2 in this medium, both the relative fluorescence of the monolayer and the proportion of cells across the monolayer that displayed calcium transients increased in a dose-dependent fashion. In conclusion, the response of an endothelial cell monolayer to increasing levels of shear is not only to increase [Ca2+]i within individual cells, but to increase the duration of response and the number of cells responding at the onset of shear. This recruitment of larger numbers of cells at higher levels of shear may represent a novel signaling mechanism within the endothelium.
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PMID:Effects of shear on endothelial cell calcium in the presence and absence of ATP. 761 66

We analyzed spatio-temporal characteristics of Ca2+ transients in the cytosol and the nucleus of cultured neonatal rat heart cells using confocal imaging with Indo-1 and Fluo-3. In resting heart muscle cells, nuclear [Ca2+] was maintained lower than the cytosolic level. The rise in nuclear [Ca2+], during either E-C coupling or propagation of the Ca2+ wave, began at the edge of the nucleus in the immediate vicinity of the rise in global or localized cytosolic [Ca2+], and spread inwardly. The rise in [Ca2+] was slower and smaller in the nucleus than in the cytosol. The decay in [Ca2+] was also slower in the nucleus than the cytosol, thereby reversing the initial [Ca2+] gradient between them. Caffeine markedly enhanced the rise in nuclear [Ca2+] while maintaining inward spreading. The heterogeneity of nuclear Ca2+ transients during cellular contractilities suggests that influx of Ca2+ from perinuclear stores into the nucleus plays a predominant role in the nuclear [Ca2+] rise. The results also indicated that spatio-temporal characteristics of Ca2+ transients are quite different between the nucleus and the cytosol, thereby suggesting that they are differentially regulated in the nucleus and the cytosol.
Cell Calcium 1995 Mar
PMID:Differences in features of calcium transients between the nucleus and the cytosol in cultured heart muscle cells: analyzed by confocal microscopy. 762 30

Effects of acetylcholine (ACh) and ATP as the candidates of efferent neurotransmitter on intracellular Ca2+ concentrations ( [Ca2+]i) of the isolated outer hair cells (OHCs) from guinea pig cochlea were studied with laser scanning confocal microscope. The OHCs were loaded with Ca2+ sensitive dye Fluo-3, whose fluorescent intensity was strongest at the basal end in resting OHC. The presence of ACh gradually increased [Ca2+]i to a higher level at the basal end of OHCs. Continuous application of ATP caused a rapid [Ca2+]i increase followed by a gradual exhaustion throughout the whole OHC. Magnitude of the increase at the apex was greater than that at the base. In OHCs whose calcium had been exhausted by ATP, ACh induced a temporary increase in [Ca2+]i. It seems likely that the ACh-induced [Ca2+]i rise is partly due to an influx of extracellular Ca2+. The bursting nature of ATP-induced [Ca2+]i rise may be a consequence of Ca2+ influx through the ATP-gated cation channels and of the mobilization of intracellular store mediated by ATP.
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PMID:[ACh and ATP induced calcium mobilization in outer hair cells of the guinea pig cochlea: confocal microscopy]. 765 85

The effects of ACh, ATP and high K+ on intracellular calcium concentration Ca2+ in outer hair cells (OHC) of the guinea pig cochleae were observed with the use of Ca2+ sensitive dye Fluo-3 and laser scanning confocal microscope. Ca2+ increase induced by these chemicals had individual temporal and spatial features. Moreover, high K+ solutions induced contraction and bending of OHC too. Taking advantage of the "optical sectioning" facility of confocal microscopy, morphography of Fluorescein-labelled living OHC and PI-dyed nuclei was reconstructed three-dimensionally. The application of confocal microscopy in OHC physiological and morphological research was discussed.
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PMID:[Confocal images of cochlear outer hair cells in the guinea pigs]. 765 18

Previous studies have shown that all-trans retinoic acid (RA) preserves fibroblast viability and stimulates their proliferation, in part, by reducing the extracellular Ca2+ requirement (Am J Pathol 1990, 130:1275). Based on this observation, we have in the present study examined the effects of RA on Ca2+ mobilization in human dermal fibroblasts. For these studies we used the Ca(2+)-binding dyes, Fluo-3 and Indo-1. Using fluorescence of Fluo-3-loaded cells or Indo-1-loaded cells as indicators of intracellular free Ca2+, we observed that treatment of the cells with RA did no, by itself, alter the concentration of intracellular Ca2+. Nor did it interfere with the rapid, transient rise in intracellular Ca2+ induced by treatment with ionomycin. However, treatment of the cells with RA prevented re-equilibration of intracellular Ca2+ when the cells were initially equilibrated in low Ca2+ (0.15 mmol/L) culture medium and then switched to high Ca2+ (1.4 mmol/L) medium or when cells were first equilibrated in high Ca2+ medium and then switched to low Ca2+ medium. This effect of RA could be seen within seconds after treatment and the effect was observed 1 day after treatment (longest time point examined). The effect was concentration dependent and concentrations of RA that modulated Ca2+ re-equilibration (0.3 to 3.0 mumol/L) were the same as those that have previously been shown to promote fibroblast survival and growth. A biologically inactive retinoid did not have this effect. Specificity of the response was suggested by the finding that concentrations of RA that modulated Ca2+ movement had no effect on Ba2+ transport. These data suggest that RA prevents re-equilibration of intracellular Ca2+ in human dermal fibroblasts by interfering with Ca2+ movement across the plasma membrane.
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PMID:All-trans retinoic acid inhibits fluctuations in intracellular Ca2+ resulting from changes in extracellular Ca2+. 767 83


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