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1

Ratan, R. R., F. R. Maxfield, and M. L. Shelanski. "Long-lasting and rapid calcium changes during mitosis." Journal of Cell Biology 107, no. 3 (1988): 993–99. http://dx.doi.org/10.1083/jcb.107.3.993.

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A more complete understanding of calcium's role in cell division requires knowledge of the timing, magnitude, and duration of changes in cytoplasmic-free calcium, [Ca2+]i, associated with specific mitotic events. To define the temporal relationship of changes in [Ca2+]i to cellular and chromosomal movements, we have measured [Ca2+]i every 6-7 s in single-dividing Pt K2 cells using fura-2 and microspectrophotometry, coupling each calcium measurement with a bright-field observation. In the 12 min before discernable chromosome some separation, 90% of metaphase cells show at least one transient of
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2

Liu, Y., S. L. Carroll, M. G. Klein, and M. F. Schneider. "Calcium transients and calcium homeostasis in adult mouse fast-twitch skeletal muscle fibers in culture." American Journal of Physiology-Cell Physiology 272, no. 6 (1997): C1919—C1927. http://dx.doi.org/10.1152/ajpcell.1997.272.6.c1919.

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Skeletal muscle fibers enzymatically dissociated from adult mouse flexor digitorum brevis muscles were maintained in culture for up to 8 days. After various times in culture, fibers were loaded with fura 2, and Ca2+ transients for trains of 1, 5, and 10 action potentials (100 Hz) triggered by external electrical stimulation were calculated from fluorescence ratio records corrected for noninstantaneous reaction of fura 2 with Ca2+. The decay rate constants of Ca2+ transients decreased with increasing stimulation duration, indicating a slowing of the Ca(2+)-removal properties with increased stim
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3

Vyshedskiy, Andrey, and Jen-Wei Lin. "Presynaptic Ca2+ Influx at the Inhibitor of the Crayfish Neuromuscular Junction: A Photometric Study at a High Time Resolution." Journal of Neurophysiology 83, no. 1 (2000): 552–62. http://dx.doi.org/10.1152/jn.2000.83.1.552.

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Presynaptic calcium influx at the inhibitor of the crayfish neuromuscular junction was investigated by measuring fluorescence transients generated by calcium-sensitive dyes. This approach allowed us to correlate presynaptic calcium influx with transmitter release at a high time resolution. Systematic testing of the calcium indicators showed that only low-affinity dyes, with affinities in the range of micromolar, should be used to avoid saturation of dye binding and interference with transmitter release. Presynaptic calcium influx was regulated by slowly increasing the duration of the action po
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4

Gidö, Gunilla, Kenichiro Katsura, Tibor Kristian, and Bo K. Siesjö. "Influence of Plasma Glucose Concentration on Rat Brain Extracellular Calcium Transients during Spreading Depression." Journal of Cerebral Blood Flow & Metabolism 13, no. 1 (1993): 179–82. http://dx.doi.org/10.1038/jcbfm.1993.21.

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The objective of this study was to establish whether tissues that are energy compromised, but not energy depleted, demonstrate exaggerated calcium transients when subjected to membrane depolarizations of the spreading depression (SD) type. Anesthetized and artificially ventilated rats were given insulin in order to induce progressively lower plasma glucose concentrations. Spreading depression was elicited by local application of KCl; extracellular calcium concentration (Ca2+e) as well as direct current (DC) potential were recorded. When plasma glucose concentration fell below ∼3 m M, the durat
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5

Wang, C., and Z. Machaty. "189 CHARACTERIZATION OF THE FIRST SPERM-INDUCED CALCIUM TRANSIENT IN PIG OOCYTES." Reproduction, Fertility and Development 28, no. 2 (2016): 225. http://dx.doi.org/10.1071/rdv28n2ab189.

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Fertilization in mammals is associated with repetitive elevations in the oocytes’ intracellular free calcium concentration. The elevations are triggered by the fertilizing sperm and are responsible for stimulating embryo development. In mouse oocytes, the sperm-induced calcium signal starts with a calcium rise that is larger and longer in duration than any succeeding transients. It also has unique characteristics: it begins with a rapid increase for 2–3 s followed by a shoulder, which is an inflection point that represents a brief decline in the rise of calcium levels. Once calcium level reach
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6

Hartmann, T., M. Kondo, H. Mochizuki, A. S. Verkman, and J. H. Widdicombe. "Calcium-dependent regulation of Cl secretion in tracheal epithelium." American Journal of Physiology-Lung Cellular and Molecular Physiology 262, no. 2 (1992): L163—L168. http://dx.doi.org/10.1152/ajplung.1992.262.2.l163.

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In primary cultures of dog tracheal epithelium, isoproterenol produced a transient increase in short-circuit current (Isc) (duration 30 s; maximal increase, 32 +/- 5 microA/cm2). This was followed by a more slowly developing sustained increase (9 +/- 3 microA/cm2), which mimicked the response to N6, 2'-O-dibutyryladenosine 3',5'-cyclic monophosphate (DBcAMP). The transient and sustained responses had dissociation constants for isoproterenol of 2 x 10(-8) and 2 x 10(-9) M, respectively. Bradykinin (in the presence of indomethacin), substance P, histamine, and thrombin produced only transient in
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7

Chaigne, Sebastien, Guillaume Cardouat, Julien Louradour, et al. "Transient receptor potential vanilloid 4 channel participates in mouse ventricular electrical activity." American Journal of Physiology-Heart and Circulatory Physiology 320, no. 3 (2021): H1156—H1169. http://dx.doi.org/10.1152/ajpheart.00497.2020.

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Transient receptor potential vanilloid 4 (TRPV4) is expressed at the membrane of mouse ventricular myocytes and colocalizes with non-T-tubular L-type calcium channels. Deletion of trpv4 gene in mice results in shortened QT interval on electrocardiogram and reduced action potential duration of ventricular myocytes. Pharmacological activation of TRPV4 channel leads to increased action potential duration and increased calcium transient amplitude in trpv4−/− but not in trpv4−/− ventricular myocytes. To the contrary, TRPV4 channel pharmacological inhibition reduces action potential duration in trpv
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8

Schneider, Eve R., Eugene F. Civillico, and Samuel S. H. Wang. "Calcium-based dendritic excitability and its regulation in the deep cerebellar nuclei." Journal of Neurophysiology 109, no. 9 (2013): 2282–92. http://dx.doi.org/10.1152/jn.00925.2012.

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The deep cerebellar nuclei (DCN) convey the final output of the cerebellum and are a major site of activity-dependent plasticity. Here, using patch-clamp recording and two-photon calcium imaging in rat brain slices, we demonstrate that DCN dendrites exhibit three hallmarks of active amplification of electrical signals. First, they produce calcium transients with rise times of tens of milliseconds, comparable in amplitude and duration to calcium spikes in other neurons. Second, calcium signal amplitudes are undiminished along the length of dendrites to the farthest distances from the soma. Thir
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9

Roome, Chris J., Emmet M. Power, and Ruth M. Empson. "Transient reversal of the sodium/calcium exchanger boosts presynaptic calcium and synaptic transmission at a cerebellar synapse." Journal of Neurophysiology 109, no. 6 (2013): 1669–80. http://dx.doi.org/10.1152/jn.00854.2012.

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The sodium/calcium exchanger (NCX) is a widespread transporter that exchanges sodium and calcium ions across excitable membranes. Normally, NCX mainly operates in its “forward” mode, harnessing the electrochemical gradient of sodium ions to expel calcium. During membrane depolarization or elevated internal sodium levels, NCX can instead switch the direction of net flux to expel sodium and allow calcium entry. Such “reverse”-mode NCX operation is frequently implicated during pathological or artificially extended periods of depolarization, not during normal activity. We have used fast calcium im
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10

Katra, Rodolphe P., Etienne Pruvot, and Kenneth R. Laurita. "Intracellular calcium handling heterogeneities in intact guinea pig hearts." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 2 (2004): H648—H656. http://dx.doi.org/10.1152/ajpheart.00374.2003.

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Regional heterogeneities of ventricular repolarizing currents and their role in arrhythmogenesis have received much attention; however, relatively little is known regarding heterogeneities of intracellular calcium handling. Because repolarization properties and contractile function are heterogeneous from base to apex of the intact heart, we hypothesize that calcium handling is also heterogeneous from base to apex. To test this hypothesis, we developed a novel ratiometric optical mapping system capable of measuring calcium fluorescence of indo-1 at two separate wavelengths from 256 sites simult
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11

Xie, Lai-Hua, and James N. Weiss. "Arrhythmogenic consequences of intracellular calcium waves." American Journal of Physiology-Heart and Circulatory Physiology 297, no. 3 (2009): H997—H1002. http://dx.doi.org/10.1152/ajpheart.00390.2009.

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Intracellular Ca2+ (Cai2+) waves are known to cause delayed afterdepolarizations (DADs), which have been associated with arrhythmias in cardiac disease states such as heart failure, catecholaminergic polymorphic ventricular tachycardia, and digitalis toxicity. Here we show that, in addition to DADs, Cai2+ waves also have other consequences relevant to arrhythmogenesis, including subcellular spatially discordant alternans (SDA, in which the amplitude of the local Cai2+ transient alternates out of phase in different regions of the same cell), sudden repolarization changes promoting the dispersio
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12

Bailey, B. A., and S. R. Houser. "Sarcoplasmic reticulum-related changes in cytosolic calcium in pressure-overload-induced feline LV hypertrophy." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 6 (1993): H2009—H2016. http://dx.doi.org/10.1152/ajpheart.1993.265.6.h2009.

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Alterations in Ca2+ homeostasis that involve the sarcoplasmic reticulum (SR) were studied in feline left ventricular (LV) myocytes isolated from hearts with LV hypertrophy induced by slow, progressive pressure overload. At death, severe hypertrophy was evidenced by increased heart weight-to-body weight ratio (8.4 +/- 0.6 vs. 4.2 +/- 0.2 g/kg in controls). Steady-state Ca2+ transients (measured as. indo 1 fluorescence at 410 nm/480 nm; I410/I480) in LV hypertrophy (LVH) myocytes had diminished peak amplitudes (I410/I480 2.28 +/- 0.07 vs. 2.53 +/- 0.07 in controls) and prolonged durations (0.75
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13

Yan, L. Y., C. Wang, H. L. Luo, and Z. Machaty. "184 INHIBITION OF CALCIUM EFFLUX EXTENDS THE DURATION OF CALCIUM SIGNALS IN PIG OOCYTES." Reproduction, Fertility and Development 24, no. 1 (2012): 204. http://dx.doi.org/10.1071/rdv24n1ab184.

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Calcium signaling involves the transient elevation in the intracellular free-calcium concentration, which is responsible for controlling a great number of biological functions. In many cell types, a signal is generated when calcium stored in the endoplasmic reticulum is released into the cytoplasm, followed by an influx of calcium across the plasma membrane. At the same time, calcium is removed from the cytosol by ATPases, which pump it back into the intracellular store or out of the cell. The size of the calcium signal is thus determined by the amount of calcium moving into and out of the cyt
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14

Crossley, I., T. Whalley, and M. Whitaker. "Guanosine 5'-thiotriphosphate may stimulate phosphoinositide messenger production in sea urchin eggs by a different route than the fertilizing sperm." Cell Regulation 2, no. 2 (1991): 121–33. http://dx.doi.org/10.1091/mbc.2.2.121.

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We show that microinjecting guanosine-5'-thiotriphosphate (GTP gamma S) into unfertilized sea urchin eggs generates an intracellular free calcium concentration [( Ca]i) transient apparently identical in magnitude and duration to the calcium transient that activates the egg at fertilization. The GTP gamma S-induced transient is blocked by prior microinjection of the inositol trisphosphate (InsP3) antagonist heparin. GTP gamma S injection also causes stimulation of the egg's Na+/H+ antiporter via protein kinase C, even in the absence of a [Ca]i increase. These data suggest that GTP gamma S acts
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15

Kapur, Sunil, Gary L. Aistrup, Rohan Sharma, et al. "Early development of intracellular calcium cycling defects in intact hearts of spontaneously hypertensive rats." American Journal of Physiology-Heart and Circulatory Physiology 299, no. 6 (2010): H1843—H1853. http://dx.doi.org/10.1152/ajpheart.00623.2010.

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Defects in excitation-contraction coupling have been reported in failing hearts, but little is known about the relationship between these defects and the development of heart failure (HF). We compared the early changes in intracellular Ca2+ cycling to those that underlie overt pump dysfunction and arrhythmogenesis found later in HF. Laser-scanning confocal microscopy was used to measure Ca2+ transients in myocytes of intact hearts in Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs) at different ages. Early compensatory mechanisms include a positive inotropic effect in SHRs at
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16

Fuchs, Andreas, Marcel Rigaud, and Quinn H. Hogan. "Painful Nerve Injury Shortens the Intracellular Ca2+ Signal in Axotomized Sensory Neurons of Rats." Anesthesiology 107, no. 1 (2007): 106–16. http://dx.doi.org/10.1097/01.anes.0000267538.72900.68.

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Abstract Background: Neuropathic pain is inadequately treated and poorly understood at the cellular level. Because intracellular Ca2+ signaling critically regulates diverse neuronal functions, the authors examined effects of peripheral nerve injury on the Ca2+ transient that follows neuronal activation. Methods: Cytoplasmic Ca2+ levels were recorded by digital microfluorometry from dissociated dorsal root ganglion neurons of hyperalgesic animals after ligation of the fifth lumbar spinal nerve and control animals. Neurons were activated by field stimulation or by K+ depolarization. Results: Tra
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17

Cinelli, Angel R., Dalton Wang, Ping Chen, Weimin Liu, and Mimi Halpern. "Calcium Transients in the Garter Snake Vomeronasal Organ." Journal of Neurophysiology 87, no. 3 (2002): 1449–72. http://dx.doi.org/10.1152/jn.00651.2001.

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The signaling cascade involved in chemosensory transduction in the VN organ is incompletely understood. In snakes, the response to nonvolatile prey chemicals is mediated by the vomeronasal (VN) system. Using optical techniques and fluorescent Ca2+ indicators, we found that prey-derived chemoattractants produce initially a transient cytosolic accumulation of [Ca2+]i in the dendritic regions of VN neurons via two pathways: Ca2+release from IP3-sensitive intracellular stores and, to a lesser extent, Ca2+ influx through the plasma membrane. Both components seem to be dependent on IP3 production. C
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18

MacGowan, Guy A., Congwu Du, Douglas B. Cowan, et al. "Ischemic dysfunction in transgenic mice expressing troponin I lacking protein kinase C phosphorylation sites." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 2 (2001): H835—H843. http://dx.doi.org/10.1152/ajpheart.2001.280.2.h835.

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To determine the in vivo functional significance of troponin I (TnI) protein kinase C (PKC) phosphorylation sites, we created a transgenic mouse expressing mutant TnI, in which PKC phosphorylation sites at serines-43 and -45 were replaced by alanine. When we used high-perfusate calcium as a PKC activator, developed pressures in transgenic (TG) perfused hearts were similar to wild-type (WT) hearts ( P = not significant, NS), though there was a 35% and 32% decrease in peak-systolic intracellular calcium ( P < 0.01) and diastolic calcium ( P < 0.005), respectively. The calcium transient dur
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19

Clusin, William T. "Mechanisms of calcium transient and action potential alternans in cardiac cells and tissues." American Journal of Physiology-Heart and Circulatory Physiology 294, no. 1 (2008): H1—H10. http://dx.doi.org/10.1152/ajpheart.00802.2007.

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Alternation of cardiac action potential duration (APD) from beat to beat and concurrent alternation of the amplitude of the calcium transient are regarded as important arrhythmia mechanisms. These phenomena are causally interrelated and can be reliably evoked by an increase in beat frequency or by ischemia. The first part of this historical review deals with the physiology of APD alternans. Sections recounting the evolution of knowledge about calcium-activated ion currents and calcium transient alternans are interspersed among sections describing the growth of the so-called “restitution hypoth
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20

Hishikawa, T., J. Y. Cheung, R. V. Yelamarty, and D. W. Knutson. "Calcium transients during Fc receptor-mediated and nonspecific phagocytosis by murine peritoneal macrophages." Journal of Cell Biology 115, no. 1 (1991): 59–66. http://dx.doi.org/10.1083/jcb.115.1.59.

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Studies with populations of macrophages have produced conflicting results concerning the possibility that the concentration of intracellular ionized calcium [( Ca2+]i) may act as an important mediator for phagocytosis. Since asynchronous changes in [Ca2+]i in individual cells undergoing phagocytosis may be averaged to undetectability in population studies, we studied single adhering murine macrophages using fura-2 and our previously described digital imaging system. The proportion of macrophages phagocytosing IgG-coated latex beads was greater than for uncoated beads (percent phagocytosing cel
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21

Whalley, T., A. McDougall, I. Crossley, K. Swann, and M. Whitaker. "Internal calcium release and activation of sea urchin eggs by cGMP are independent of the phosphoinositide signaling pathway." Molecular Biology of the Cell 3, no. 3 (1992): 373–83. http://dx.doi.org/10.1091/mbc.3.3.373.

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We show that microinjecting cyclic GMP (cGMP) into unfertilized sea urchin eggs activates them by stimulating a rise in the intracellular free calcium ion concentration ([Ca2+]i). The increase in [Ca2+]i is similar in both magnitude and duration to the transient that activates the egg at fertilization. It is due to mobilization of calcium from intracellular stores but is not prevented by the inositol trisphosphate (InsP3) antagonist heparin. Furthermore, cGMP does not stimulate the eggs Na+/H+ antiport when the [Ca2+]i transient is blocked by the calcium chelator bis-(O-aminophenoxy)-N,N,N',N'
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22

Fisher, T. E., S. Levy, and L. K. Kaczmarek. "Transient changes in intracellular calcium associated with a prolonged increase in excitability in neurons of Aplysia californica." Journal of Neurophysiology 71, no. 3 (1994): 1254–57. http://dx.doi.org/10.1152/jn.1994.71.3.1254.

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1. Transient stimulation of an afferent input to the bag cell neurons of Aplysia californica triggers a 30-min period of spontaneous firing termed the afterdischarge. Measurement of free calcium ion concentrations using calcium-sensitive electrodes revealed a biphasic pattern of elevation of intracellular calcium levels during the afterdischarge. Basal calcium levels at the soma were found to rise rapidly during afferent stimulation and then to decline before the onset of spontaneous firing. This early peak in intracellular calcium was followed by a slower, transient elevation of calcium level
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23

Zbicz, K. L., and F. F. Weight. "Transient voltage and calcium-dependent outward currents in hippocampal CA3 pyramidal neurons." Journal of Neurophysiology 53, no. 4 (1985): 1038–58. http://dx.doi.org/10.1152/jn.1985.53.4.1038.

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Membrane currents activated by step changes in membrane potential were studied in hippocampal pyramidal neurons of region CA3 using the single microelectrode voltage-clamp technique. The transient outward current activated by depolarizing steps appeared to be composed of two transient currents that could be distinguished by differences in voltage sensitivity, time course, and pharmacological sensitivity. The more slowly decaying current was activated by voltage steps positive to -60 mV and declined exponentially with a time constant between 200 and 400 ms. This current inactivated as the holdi
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24

Pioner, Josè Manuel, Lorenzo Santini, Chiara Palandri, et al. "Optical Investigation of Action Potential and Calcium Handling Maturation of hiPSC-Cardiomyocytes on Biomimetic Substrates." International Journal of Molecular Sciences 20, no. 15 (2019): 3799. http://dx.doi.org/10.3390/ijms20153799.

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Cardiomyocytes from human induced pluripotent stem cells (hiPSC-CMs) are the most promising human source with preserved genetic background of healthy individuals or patients. This study aimed to establish a systematic procedure for exploring development of hiPSC-CM functional output to predict genetic cardiomyopathy outcomes and identify molecular targets for therapy. Biomimetic substrates with microtopography and physiological stiffness can overcome the immaturity of hiPSC-CM function. We have developed a custom-made apparatus for simultaneous optical measurements of hiPSC-CM action potential
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25

Thompson, S. M., and D. A. Prince. "Activation of electrogenic sodium pump in hippocampal CA1 neurons following glutamate-induced depolarization." Journal of Neurophysiology 56, no. 2 (1986): 507–22. http://dx.doi.org/10.1152/jn.1986.56.2.507.

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Intracellular recordings were obtained from guinea pig hippocampal CA1 pyramidal neurons maintained in vitro. Focal applications of glutamate produced depolarizations followed by prolonged hyperpolarizations. The mechanisms underlying this postglutamate hyperpolarization (PGH) were investigated. PGH did not reverse polarity with hyperpolarization to potentials at or near the presumed K+ equilibrium potential. A transient increase in conductance was associated with the PGH; control values returned well before the termination of PGH. Application of Mn2+, an antagonist of voltage-dependent calciu
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26

Paudel, Roshan, Mohsin Saleet Jafri, and Aman Ullah. "The Role of Ca2+ Sparks in Force Frequency Relationships in Guinea Pig Ventricular Myocytes." Biomolecules 12, no. 11 (2022): 1577. http://dx.doi.org/10.3390/biom12111577.

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Calcium sparks are the elementary Ca2+ release events in excitation-contraction coupling that underlie the Ca2+ transient. The frequency-dependent contractile force generated by cardiac myocytes depends upon the characteristics of the Ca2+ transients. A stochastic computational local control model of a guinea pig ventricular cardiomyocyte was developed, to gain insight into mechanisms of force-frequency relationship (FFR). This required the creation of a new three-state RyR2 model that reproduced the adaptive behavior of RyR2, in which the RyR2 channels transition into a different state when e
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27

Chen, Y., X. D. Sun, and S. Herness. "Characteristics of action potentials and their underlying outward currents in rat taste receptor cells." Journal of Neurophysiology 75, no. 2 (1996): 820–31. http://dx.doi.org/10.1152/jn.1996.75.2.820.

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1. Taste receptor cells produce action potentials as a result of transduction mechanisms that occur when these cells are stimulated with tastants. These action potentials are thought to be key signaling events in relaying information to the central nervous system. We explored the ionic basis of action potentials from dissociated posterior rat taste cells using the patch-clamp recording technique in both voltage-clamp and current-clamp modes. 2. Action potentials were evoked by intracellular injection of depolarizing current pulses from a holding potential of -80 mV. The threshold potential for
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28

Lin, Eric, Calvin Craig, Marcel Lamothe, Marinko V. Sarunic, Mirza Faisal Beg, and Glen F. Tibbits. "Construction and use of a zebrafish heart voltage and calcium optical mapping system, with integrated electrocardiogram and programmable electrical stimulation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 308, no. 9 (2015): R755—R768. http://dx.doi.org/10.1152/ajpregu.00001.2015.

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Zebrafish are increasingly being used as a model of vertebrate cardiology due to mammalian-like cardiac properties in many respects. The size and fecundity of zebrafish make them suitable for large-scale genetic and pharmacological screening. In larger mammalian hearts, optical mapping is often used to investigate the interplay between voltage and calcium dynamics and to investigate their respective roles in arrhythmogenesis. This report outlines the construction of an optical mapping system for use with zebrafish hearts, using the voltage-sensitive dye RH 237 and the calcium indicator dye Rho
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29

ten Tusscher, K. H. W. J., D. Noble, P. J. Noble, and A. V. Panfilov. "A model for human ventricular tissue." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 4 (2004): H1573—H1589. http://dx.doi.org/10.1152/ajpheart.00794.2003.

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The experimental and clinical possibilities for studying cardiac arrhythmias in human ventricular myocardium are very limited. Therefore, the use of alternative methods such as computer simulations is of great importance. In this article we introduce a mathematical model of the action potential of human ventricular cells that, while including a high level of electrophysiological detail, is computationally cost-effective enough to be applied in large-scale spatial simulations for the study of reentrant arrhythmias. The model is based on recent experimental data on most of the major ionic curren
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30

Frasier, Chad R., Jacy L. Wagnon, Yangyang Oliver Bao, et al. "Cardiac arrhythmia in a mouse model of sodium channel SCN8A epileptic encephalopathy." Proceedings of the National Academy of Sciences 113, no. 45 (2016): 12838–43. http://dx.doi.org/10.1073/pnas.1612746113.

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Patients with early infantile epileptic encephalopathy (EIEE) are at increased risk for sudden unexpected death in epilepsy (SUDEP). De novo mutations of the sodium channel gene SCN8A, encoding the sodium channel Nav1.6, result in EIEE13 (OMIM 614558), which has a 10% risk of SUDEP. Here, we investigated the cardiac phenotype of a mouse model expressing the gain of function EIEE13 patient mutation p.Asn1768Asp in Scn8a (Nav1.6-N1768D). We tested Scn8aN1768D/+ mice for alterations in cardiac excitability. We observed prolongation of the early stages of action potential (AP) repolarization in mu
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31

Saegusa, Noriko, Vivek Garg, and Kenneth W. Spitzer. "Modulation of ventricular transient outward K+ current by acidosis and its effects on excitation-contraction coupling." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 12 (2013): H1680—H1696. http://dx.doi.org/10.1152/ajpheart.00070.2013.

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The contribution of transient outward current ( Ito) to changes in ventricular action potential (AP) repolarization induced by acidosis is unresolved, as is the indirect effect of these changes on calcium handling. To address this issue we measured intracellular pH (pHi), Ito, L-type calcium current ( ICa,L), and calcium transients (CaTs) in rabbit ventricular myocytes. Intracellular acidosis [pHi 6.75 with extracellular pH (pHo) 7.4] reduced Ito by ∼50% in myocytes with both high (epicardial) and low (papillary muscle) Ito densities, with little effect on steady-state inactivation and activat
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32

Hayashi, H., T. Watanabe, and T. F. McDonald. "Action potential duration in ventricular muscle during selective metabolic block." American Journal of Physiology-Heart and Circulatory Physiology 253, no. 2 (1987): H373—H379. http://dx.doi.org/10.1152/ajpheart.1987.253.2.h373.

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We have examined whether maintenance of the cardiac action potential duration depends exclusively on energy from glycolysis. Oxidative phosphorylation in guinea pig papillary muscles was inhibited by superfusion with hypoxic solutions. After 60 min in 50 mM glucose solution, the action potential duration was 85% of aerobic control, but ATP content was only 25%; after 60 min in 0 mM glucose, both the duration and ATP content had declined to 15% control. When the glucose concentration of hypoxic solution was raised from 0 to 50 mM, there was nearly full recovery of the action potential duration
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33

Ruiz-Petrich, Elena, and Normand Leblanc. "The mechanism of the rate-dependent changes of the conducted action potential in rabbit ventricle." Canadian Journal of Physiology and Pharmacology 67, no. 7 (1989): 780–87. http://dx.doi.org/10.1139/y89-124.

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Blockers of the transient outward current (4-aminopyridine) and the Ca current (Co2+) as well as injection of polarizing current during the plateau were used to assess the role of these current systems as determinants of action potential duration at different pacing rates. Papillary muscles and ventricular trabecula were superfused with oxygenated Krebs solution at 33 °C and driven at a basic rate of 1 Hz. The effects of varying the frequency of stimulation between 0.1 and 4 Hz on action potential parameters were determined under control conditions and during exposure to 2 mM 4-aminopyridine,
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34

Livshitz, Leonid, Keith Decker, Gregory Faber, Thomas O'Hara, Jonathan Silva, and Yoram Rudy. "Comments on “A model for human ventricular tissue”." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 1 (2005): H453. http://dx.doi.org/10.1152/ajpheart.00826.2004.

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The experimental and clinical possibilities for studying cardiac arrhythmias in human ventricular myocardium are very limited. Therefore, the use of alternative methods such as computer simulations is of great importance. In this article we introduce a mathematical model of the action potential of human ventricular cells that, while including a high level of electrophysiological detail, is computationally cost-effective enough to be applied in large-scale spatial simulations for the study of reentrant arrhythmias. The model is based on recent experimental data on most of the major ionic curren
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35

Martins, Eduardo, Kenji Inamura, Klas Themner, Klas G. Malmqvist, and Bo K. Siesjö. "Accumulation of Calcium and Loss of Potassium in the Hippocampus following Transient Cerebral Ischemia: A Proton Microprobe Study." Journal of Cerebral Blood Flow & Metabolism 8, no. 4 (1988): 531–38. http://dx.doi.org/10.1038/jcbfm.1988.93.

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This study explored (a) whether postischemic accumulation of calcium in hippocampal neurons precedes or occurs pari passu with light microscopical signs of delayed neuronal necrosis, and (b) whether calcium initially accumulates in dendritic domains, presumed to have a high density of agonist-operated calcium channels. Transient ischemia of 10-min duration was induced in rats, and the animals were studied after 1, 2, 3, and 4 days of recovery. We measured total calcium and potassium contents in the stratum oriens, pyramidale, radiatum, and moleculare of the CA1 and CA3 sectors, using particle
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36

Nguyen, My-Hanh T., S. J. Dudycha, and M. Saleet Jafri. "Effect of Ca2+ on cardiac mitochondrial energy production is modulated by Na+ and H+ dynamics." American Journal of Physiology-Cell Physiology 292, no. 6 (2007): C2004—C2020. http://dx.doi.org/10.1152/ajpcell.00271.2006.

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The energy production of mitochondria in heart increases during exercise. Several works have suggested that calcium acts at multiple control points to activate net ATP production in what is termed “parallel activation”. To study this, a computational model of mitochondrial energy metabolism in the heart has been developed that integrates the Dudycha-Jafri model for the tricarboxylic acid cycle with the Magnus-Keizer model for mitochondrial energy metabolism and calcium dynamics. The model improves upon the previous formulation by including an updated formulation for calcium dynamics, and new d
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37

Hilgemann, D. W. "Extracellular calcium transients at single excitations in rabbit atrium measured with tetramethylmurexide." Journal of General Physiology 87, no. 5 (1986): 707–35. http://dx.doi.org/10.1085/jgp.87.5.707.

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Extracellular calcium transients were resolved within the time course of single contraction cycles in rabbit left atrium using tetramethylmurexide (2 mM) as the calcium-sensitive dye (150-250 microM total calcium, 80-150 microM free calcium). Net extracellular calcium depletion began within 2-4 ms upon excitation; over the following 5-20 ms, depletion continued steeply and amounted to 0.2 mumol/kg wet weight X 10 ms (135 microM free extracellular calcium). In regularly excited muscles (0.5-2 Hz), net depletion slowed rapidly and stopped early during the rise of contractile motion monitored by
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38

Zaniboni, Massimiliano. "Ventricular Repolarization and Calcium Transient Show Resonant Behavior under Oscillatory Pacing Rate." Biomolecules 12, no. 7 (2022): 873. http://dx.doi.org/10.3390/biom12070873.

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Cardiac EC coupling is triggered by rhythmic depolarizing current fronts originating from the sino-atrial node, and the way variability in rhythm is associated with variability in action potential duration (APD) and, in turn, in the variability of calcium transient amplitude (CTA) and contraction is a key determinant of beating stability. Sinusoidal-varying pacing rate is adopted here in order to establish whether APD and CTA oscillations, elicited in a human ventricular AP model (OR) under oscillatory pacing, are consistent with the dynamics of two coupled harmonic oscillators, e.g., a two-de
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39

Blackwell, K. T. "Calcium Waves and Closure of Potassium Channels in Response to GABA Stimulation in Hermissenda Type B Photoreceptors." Journal of Neurophysiology 87, no. 2 (2002): 776–92. http://dx.doi.org/10.1152/jn.00867.2000.

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Classical conditioning of Hermissenda crassicornisrequires the paired presentation of a conditioned stimulus (light) and an unconditioned stimulus (turbulence). Light stimulation of photoreceptors leads to production of diacylglycerol, an activator of protein kinase C, and inositol triphosphate (IP3), which releases calcium from intracellular stores. Turbulence causes hair cells to release GABA onto the terminal branches of the type B photoreceptor. One prior study has shown that GABA stimulation produces a wave of calcium that propagates from the terminal branches to the soma and raises the p
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40

Klos, Matthew L., Wanqing Hou, Bernard Nsengimana, et al. "Differential Effects of Beta-Hydroxybutyrate Enantiomers on Induced Pluripotent Stem Derived Cardiac Myocyte Electrophysiology." Biomolecules 12, no. 10 (2022): 1500. http://dx.doi.org/10.3390/biom12101500.

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Beta-hydroxybutyrate (βOHB), along with acetoacetate and acetone, are liver-produced ketone bodies that are increased after fasting or prolonged exercise as an alternative fuel source to glucose. βOHB, as the main circulating ketone body, is not only a G-protein coupled receptor ligand but also a histone deacetylases inhibitor, prompting the reexamination of its role in health and disease. In this study, we compared the effects of two commercial βOHB formulations an enantiomer R βOHB and a racemic mixture ± βOHB on induced pluripotent stem cell cardiac myocytes (iPS-CMs) electrophysiology. Car
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41

Ma, Jiying, and Dongmei Xiao. "Nonlinear dynamics of a mathematical model on action potential duration and calcium transient in paced cardiac cells." Discrete & Continuous Dynamical Systems - B 18, no. 9 (2013): 2377–96. http://dx.doi.org/10.3934/dcdsb.2013.18.2377.

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42

Srivastava, Shekhar, Leon Collis, Anita Go, Salvatore Mancarella, William A. Coetzee, and Michael Artman. "Paradoxical Effect of Dofetilide on Action Potential Duration and Calcium Transient Amplitude in Newborn Rabbit Ventricular Myocytes." Journal of Cardiovascular Pharmacology 45, no. 2 (2005): 165–74. http://dx.doi.org/10.1097/01.fjc.0000151896.57637.66.

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43

Greenstein, Joseph L., Richard Wu, Sunny Po, Gordon F. Tomaselli, and Raimond L. Winslow. "Role of the Calcium-Independent Transient Outward Current I to1 in Shaping Action Potential Morphology and Duration." Circulation Research 87, no. 11 (2000): 1026–33. http://dx.doi.org/10.1161/01.res.87.11.1026.

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44

Lee, Hsiang-Chun, Chi Wei, Liang-Yin Ke, et al. "Atherogenic Very-Low-Density Lipoprotein Shortens Atrial Action Potential Duration by Increasing Potassium Currents and Calcium Transient." Biophysical Journal 108, no. 2 (2015): 586a. http://dx.doi.org/10.1016/j.bpj.2014.11.3196.

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45

Lacombe, Véronique A., Serge Viatchenko-Karpinski, Dmitry Terentyev, et al. "Mechanisms of impaired calcium handling underlying subclinical diastolic dysfunction in diabetes." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 5 (2007): R1787—R1797. http://dx.doi.org/10.1152/ajpregu.00059.2007.

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Isolated diastolic dysfunction is found in almost half of asymptomatic patients with well-controlled diabetes and may precede diastolic heart failure. However, mechanisms that underlie diastolic dysfunction during diabetes are not well understood. We tested the hypothesis that isolated diastolic dysfunction is associated with impaired myocardial Ca2+ handling during type 1 diabetes. Streptozotocin-induced diabetic rats were compared with age-matched placebo-treated rats. Global left ventricular myocardial performance and systolic function were preserved in diabetic animals. Diabetes-induced di
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46

Payne, Richard J., Marc A. Tewfik, Michael P. Hier, et al. "Benefits Resulting from 1-and 6-Hour Parathyroid Hormone and Calcium Levels After Thyroidectomy." Otolaryngology–Head and Neck Surgery 133, no. 3 (2005): 386–90. http://dx.doi.org/10.1016/j.otohns.2005.02.021.

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OBJECTIVE: Previous studies have established the efficacy of post-thyroidectomy hypocalcemia monitoring using parathyroid hormone (PTH) and corrected calcium levels at 1 and 6 hours. The goal of this study was to measure the impact of managing patients based on the above findings with respect to: duration of hospital stays, rates of transient hypocalcemia, number of blood tests, cost savings, and discharge from the hospital as early as 8 hours post-thyroidectomy without compromising safety. STUDY DESIGN AND SETTING: This is a prospective study involving 95 total thyroidectomy patients using hi
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47

Nashat, Amir H., and Robert Langer. "Temporal Characteristics of Activation, Deactivation, and Restimulation of Signal Transduction following Depolarization in the Pheochromocytoma Cell Line PC12." Molecular and Cellular Biology 23, no. 14 (2003): 4788–95. http://dx.doi.org/10.1128/mcb.23.14.4788-4795.2003.

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ABSTRACT This study focuses on the transient and dynamic activation of intracellular signal transduction following different protocols of depolarization. During chronic depolarization, phosphorylation of extracellular signal-regulated kinases (ERKs) was observed to peak and subsequently fall to low levels within 10 min of depolarization. Short periods of depolarization, from 1 to 5 min in duration, also led to phosphorylation of ERK, and the rate of ERK dephosphorylation was not affected by the duration of depolarization. Phosphorylation of the cyclic AMP response element binding protein (CREB
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48

Munzenmaier, D. H., and A. S. Greene. "Angiotensin II mediates a sustained rise in nuclear and cytoplasmic calcium via multiple receptor subtypes." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 2 (1995): H565—H570. http://dx.doi.org/10.1152/ajpheart.1995.269.2.h565.

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Alterations in nuclear calcium levels in response to angiotensin II (ANG II) may play an important role in the trophic actions of ANG II. This study utilized confocal microscopy and nuclear staining to test the hypothesis that both nuclear and cytoplasmic calcium levels are altered in response to ANG II stimulation of freshly dissociated aortic smooth muscle cells. Cells were loaded with the calcium indicator fluo 3 acetoxymethyl ester, and the calcium response to ANG II stimulation was analyzed over time with a laser-scanning confocal microscope. Additionally, the ratiometric calcium indicato
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49

Hirose, R., and E. B. Chang. "Effects of serotonin on Na+-H+ exchange and intracellular calcium in isolated chicken enterocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no. 6 (1988): G891—G897. http://dx.doi.org/10.1152/ajpgi.1988.254.6.g891.

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The effects of serotonin or 5-hydroxytryptamine (5-HT) on Na absorption and intracellular free Ca (Cai) in isolated chicken enterocytes was examined. The rate of initial 22Na uptake was inhibited by 50% after 90 s of stimulation with 5-HT (10(-5) M), an effect that was not additive with amiloride (10(-3) M) and was transient (less than 10 min). 5-HT similarly decreased intracellular pH (pHi) in cells loaded with the pH indicator carboxyfluorescein, an effect that was also transient, not additive with amiloride, and Na dependent. The ED50 of this effect was approximately 10(-8) M. 5-HT also sti
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50

Tsuchida, Katsuharu, and Hiroshi Watajima. "Potassium currents in ventricular myocytes from genetically diabetic rats." American Journal of Physiology-Endocrinology and Metabolism 273, no. 4 (1997): E695—E700. http://dx.doi.org/10.1152/ajpendo.1997.273.4.e695.

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Our previous study demonstrated the longer duration of action potential in ventricular myocytes from genetically diabetic WBN/Kob rats without change in calcium channel density compared with age-matched controls [Tsuchida, K., H. Watajima, and S. Otamo. Am. J. Physiol. 267 ( Heart Circ. Physiol. 36): H2280–H2289, 1994]. In the present study we examined the alteration of potassium currents, especially transient outward current, in ventricular myocytes of genetically diabetic WBN/Kob rats. WBN/Kob rats gradually develop hyperglycemia with aging and show some similarity to non-insulin-dependent d
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