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Cytoplasmic Ca2+ (cytoplasmic + ca2+)

Distribution by Scientific Domains
Life Sciences66%

Terms modified by Cytoplasmic Ca2+

  • cytoplasmic ca2+ concentration
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    Selected Abstracts

    AMPA/kainate and NMDA-like glutamate receptors at the chromatophore neuromuscular junction of the squid: role in synaptic transmission and skin patterning

    EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 3 2003
    Pedro A. Lima
    Abstract Glutamate receptor types were examined at the chromatophore synapses of the squids Alloteuthis subulata and Loligo vulgaris, where nerve-induced muscle contraction causes chromatophore expansion. Immunoblotting with antibody raised against a squid AMPA receptor (sGluR) demonstrated that AMPA/kainate receptors are present in squid skin. Application of l -glutamate evoked chromatophore muscle contractions in both ventral and dorsal skins, while NMDA was only active on a subpopulation of dorsal chromatophores. In dorsal skin, neurotransmission was partly blocked by either AMPA/kainate receptor antagonists (CNQX and DNQX) or NMDA receptor antagonists (AP-5 and MK-801) or completely blocked by simultaneous application of both classes of antagonists. In isolated muscle fibres, ionophoretic application of l -glutamate evoked fast inward CNQX- and DNQX-sensitive currents with reversal potentials around +14 mV and a high conductance to Na+. In fibres from dorsal skin only, a slower outward glutamate-sensitive current appeared at positive holding potentials. At negative potentials, currents were potentiated by glycine or by removing external Mg2+ and were blocked by AP-5 and MK-801. Glutamate caused a fast, followed by a slow, transient increase in cytoplasmic Ca2+. The slow component was increased in amplitude and duration by glycine or by lowering external Mg2+ and decreased by AP-5 and MK-801. In cells from ventral skin, no ,NMDA-like responses' were detected. Thus, while AMPA/kainate receptors mediated fast excitatory synaptic transmission and rapid colour change over the whole skin, activation of both AMPA/kainate and NMDA-like receptors in a subpopulation of dorsal chromatophores prolonged the postsynaptically evoked Ca2+ elevation causing temporally extended colour displays with behavioural significance. [source]

    The role of calcium in apoptosis induced by 7,-hydroxycholesterol and cholesterol-5,,6,-epoxide

    JOURNAL OF BIOCHEMICAL AND MOLECULAR TOXICOLOGY, Issue 5 2009
    Sinéad Lordan
    Abstract Oxysterols, such as 7,-hydroxy-cholesterol (7,-OH) and cholesterol-5,,6,-epoxide (,-epoxide), may have a central role in promoting atherogenesis. This is thought to be predominantly due to their ability to induce apoptosis in cells of the vascular wall and in monocytes/macrophages. Although there has been extensive research regarding the mechanisms through which oxysterols induce apoptosis, much remains to be clarified. Given that experimental evidence has long associated alterations of calcium (Ca2+) homeostasis to apoptotic cell death, the aim of the present study was to determine the influence of intracellular Ca2+ changes on apoptosis induced by 7,-OH and ,-epoxide. Ca2+ responses in differentiated U937 cells were assessed by epifluorescence video microscopy, using the ratiometric dye fura-2. Over 15-min exposure of differentiated U937 cells to 30 ,M of 7,-OH induced a slow but significant rise in fura-2 ratio. The Ca2+ channel blocker nifedipine and the chelating agent EGTA blocked the increase in cytoplasmic Ca2+. Moreover, dihydropyridine (DHP) binding sites identified with BODIPY-FLX-DHP were blocked following pretreatment with nifedipine, indicating that the influx of Ca2+ occurred through L-type channels. However, following long-term incubation with 7,-OH, elevated levels of cytoplasmic Ca2+ were not maintained and nifedipine did not provide protection against apoptotic cell death. Our results indicate that the increase in Ca2+ may be an initial trigger of 7,-OH,induced apoptosis, but following chronic exposure to the oxysterol, the influence of Ca2+ on apoptotic cell death appears to be less significant. In contrast, Ca2+ did not appear to be involved in ,-epoxide,induced apoptosis. © 2009 Wiley Periodicals, Inc. J Biochem Mol Toxicol 23:324,332, 2009; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.20295 [source]

    Uterine Expression of Epidermal Growth Factor Family During the Course of Pregnancy in Pigs

    REPRODUCTION IN DOMESTIC ANIMALS, Issue 5 2009
    Y-J Kim
    Contents To stably maintain pregnancy, several genes are expressed in the uterus. In particular, the endometrial expression of genes encoding growth factors appears to play a key role in maternal,foetal communication. The previous studies characterized the endometrial expression kinetics of the genes encoding epidermal growth factor (EGF), its receptor (EGFR), transforming growth factor-alpha (TGF-,), amphiregulin (Areg), heparin-binding (Hb) EGF and calbindin-D9k (CaBP-9k) in pigs during implantation. Here, we further characterized the expression patterns of these molecules during the entire porcine pregnancy. Porcine uteri were collected at pregnancy days (PD) 12, 15, 30, 60, 90 and 110 and subjected to RT-PCR. EGF and EGFR showed similar expression patterns, being highly expressed around implantation and then disappearing. TGF-, and Areg expression levels rose steadily until they peaked at PD30, after which they gradually decreased to PD12 levels. This Areg mRNA expression pattern was confirmed by real-time PCR and similar Areg protein expression patterns were observed. Immunohistochemical analysis of PD60 uteri revealed Areg in the glandular and luminal epithelial cells. Hb EGF was steadily expressed throughout the entire pregnancy, while CaBP-9k was expressed strongly on PD12, and then declined sharply on PD15 before recovering slightly for the remainder of the pregnancy. Thus, the EGF family may play a key role during implantation in pigs. In addition, CaBP-9k may help to maintain uterine quiescence during pregnancy by sequestering cytoplasmic Ca2+. [source]

    Role of mitochondria in modulation of spontaneous Ca2+ waves in freshly dispersed interstitial cells of Cajal from the rabbit urethra

    THE JOURNAL OF PHYSIOLOGY, Issue 19 2008
    Gerard P. Sergeant
    Interstitial cells of Cajal (ICC) isolated from the rabbit urethra exhibit pacemaker activity that results from spontaneous Ca2+ waves. The purpose of this study was to investigate if this activity was influenced by Ca2+ uptake into mitochondria. Spontaneous Ca2+ waves were recorded using a Nipkow spinning disk confocal microscope and spontaneous transient inward currents (STICs) were recorded using the whole-cell patch clamp technique. Disruption of the mitochondrial membrane potential with the electron transport chain inhibitors rotenone (10 ,m) and antimycin A (5 ,m) abolished Ca2+ waves and increased basal Ca2+ levels. Similar results were achieved when mitochondria membrane potential was collapsed using the protonophores FCCP (0.2 ,m) and CCCP (1 ,m). Spontaneous Ca2+ waves were not inhibited by the ATP synthase inhibitor oligomycin (1 ,m), suggesting that these effects were not attributable to an effect on ATP levels. STICs recorded under voltage clamp at ,60 mV were also inhibited by CCCP and antimycin A. Dialysis of cells with the mitochondrial uniporter inhibitor RU360 (10 ,m) also inhibited STICS. Stimulation of Ca2+ uptake into mitochondria using the plant flavonoid kaempferol (10 ,m) induced a series of propagating Ca2+ waves. The kaempferol-induced activity was inhibited by application of caffeine (10 mm) or removal of extracellular Ca2+, but was not significantly affected by the IP3 receptor blocker 2-APB (100 ,m). These data suggest that spontaneous Ca2+ waves in urethral ICC are regulated by buffering of cytoplasmic Ca2+ by mitochondria. [source]

    Ca2+ microdomains near plasma membrane Ca2+ channels: impact on cell function

    THE JOURNAL OF PHYSIOLOGY, Issue 13 2008
    Anant B. Parekh
    In eukaryotic cells, a rise in cytoplasmic Ca2+ can activate a plethora of responses that operate on time scales ranging from milliseconds to days. Inherent to the use of a promiscuous signal like Ca2+ is the problem of specificity: how can Ca2+ activate some responses but not others? We now know that the spatial profile of the Ca2+ signal is important Ca2+ does not simply rise uniformly throughout the cytoplasm upon stimulation but can reach very high levels locally, creating spatial gradients. The most fundamental local Ca2+ signal is the Ca2+ microdomain that develops rapidly near open plasmalemmal Ca2+ channels like voltage-gated L-type (Cav1.2) and store-operated CRAC channels. Recent work has revealed that Ca2+ microdomains arising from these channels are remarkably versatile in triggering a range of responses that differ enormously in both temporal and spatial profile. Here, I delineate basic features of Ca2+ microdomains and then describe how these highly local signals are used by Ca2+ -permeable channels to drive cellular responses. [source]

    G protein-independent neuromodulatory action of adenosine on metabotropic glutamate signalling in mouse cerebellar Purkinje cells

    THE JOURNAL OF PHYSIOLOGY, Issue 2 2007
    Toshihide Tabata
    Adenosine receptors (ARs) are G protein-coupled receptors (GPCRs) mediating the neuromodulatory actions of adenosine that influence emotional, cognitive, motor, and other functions in the central nervous system (CNS). Previous studies show complex formation between ARs and metabotropic glutamate receptors (mGluRs) in heterologous systems and close colocalization of ARs and mGluRs in several central neurons. Here we explored the possibility of intimate functional interplay between Gi/o protein-coupled A1 -subtype AR (A1R) and type-1 mGluR (mGluR1) naturally occurring in cerebellar Purkinje cells. Using a perforated-patch voltage-clamp technique, we found that both synthetic and endogenous agonists for A1R induced continuous depression of a mGluR1-coupled inward current. A1R agonists also depressed mGluR1-coupled intracellular Ca2+ mobilization monitored by fluorometry. A1R indeed mediated this depression because genetic depletion of A1R abolished it. Surprisingly, A1R agonist-induced depression persisted after blockade of Gi/o protein. The depression appeared to involve neither the cAMP-protein kinase A cascade downstream of the alpha subunits of Gi/o and Gs proteins, nor cytoplasmic Ca2+ that is suggested to be regulated by the beta-gamma subunit complex of Gi/o protein. Moreover, A1R did not appear to affect Gq protein which mediates the mGluR1-coupled responses. These findings suggest that A1R modulates mGluR1 signalling without the aid of the major G proteins. In this respect, the A1R-mediated depression of mGluR1 signalling shown here is clearly distinguished from the A1R-mediated neuronal responses described so far. These findings demonstrate a novel neuromodulatory action of adenosine in central neurons. [source]