Literatura académica sobre el tema "EGTA-AM"
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Artículos de revistas sobre el tema "EGTA-AM"
Pryor, Paul R., Barbara M. Mullock, Nicholas A. Bright, Sally R. Gray y J. Paul Luzio. "The Role of Intraorganellar Ca2+In Late Endosome–Lysosome Heterotypic Fusion and in the Reformation of Lysosomes from Hybrid Organelles". Journal of Cell Biology 149, n.º 5 (29 de mayo de 2000): 1053–62. http://dx.doi.org/10.1083/jcb.149.5.1053.
Texto completoReyes, Fredy D. y Edgar T. Walters. "Long-Lasting Synaptic Potentiation Induced by Depolarization Under Conditions That Eliminate Detectable Ca2+ Signals". Journal of Neurophysiology 103, n.º 3 (marzo de 2010): 1283–94. http://dx.doi.org/10.1152/jn.00704.2009.
Texto completoWU, Qiang-Sheng, Qiu-Dan NI, Yan-Cong QUE y Wei HUANG. "Calcium and Calmodulin Involve in Mycorrhizal and Root Development in Trifoliate Orange Colonized by Rhizophagus intraradices". Notulae Botanicae Horti Agrobotanici Cluj-Napoca 42, n.º 2 (2 de diciembre de 2014): 380–85. http://dx.doi.org/10.15835/nbha4229635.
Texto completoMiteva, Anna, Alexander Gaydukov y Olga Balezina. "Interaction between Calcium Chelators and the Activity of P2X7 Receptors in Mouse Motor Synapses". International Journal of Molecular Sciences 21, n.º 6 (16 de marzo de 2020): 2034. http://dx.doi.org/10.3390/ijms21062034.
Texto completoJohnson, J. D., Y. Jiang y M. Flynn. "Modulation of Ca2+ transients and tension by intracellular EGTA in intact frog muscle fibers". American Journal of Physiology-Cell Physiology 272, n.º 5 (1 de mayo de 1997): C1437—C1444. http://dx.doi.org/10.1152/ajpcell.1997.272.5.c1437.
Texto completoUemura, Naomi, Kenneth E. J. Dickinson, Yuji Horiguchi, Haruki Matsumoto y Basil I. Hirschowitz. "Decreased secretion due to a Ca2+ influx defect in frog peptic cells isolated with EGTA". American Journal of Physiology-Gastrointestinal and Liver Physiology 258, n.º 4 (1 de abril de 1990): G542—G551. http://dx.doi.org/10.1152/ajpgi.1990.258.4.g542.
Texto completoYoo, Je-Ok, Chang-Hee Lee, Byeong-Moon Hwang, Woo Jin Kim, Young-Myeong Kim y Kwon-Soo Ha. "Regulation of intracellular Ca2+ in the cytotoxic response to photodynamic therapy with a chlorin-based photosensitizer". Journal of Porphyrins and Phthalocyanines 13, n.º 07 (julio de 2009): 811–17. http://dx.doi.org/10.1142/s1088424609001066.
Texto completoMaloney, Judith A., Oxana M. Tsygankova, Lijun Yang, Qiuyang Li, Agnieszka Szot, Kemal Baysal y John R. Williamson. "Activation of ERK by Ca2+store depletion in rat liver epithelial cells". American Journal of Physiology-Cell Physiology 276, n.º 1 (1 de enero de 1999): C221—C230. http://dx.doi.org/10.1152/ajpcell.1999.276.1.c221.
Texto completoIchimura, Hideo, Kaushik Parthasarathi, Jens Lindert y Jahar Bhattacharya. "Lung surfactant secretion by interalveolar Ca2+ signaling". American Journal of Physiology-Lung Cellular and Molecular Physiology 291, n.º 4 (octubre de 2006): L596—L601. http://dx.doi.org/10.1152/ajplung.00036.2006.
Texto completoFeller, M. B., K. R. Delaney y D. W. Tank. "Presynaptic calcium dynamics at the frog retinotectal synapse". Journal of Neurophysiology 76, n.º 1 (1 de julio de 1996): 381–400. http://dx.doi.org/10.1152/jn.1996.76.1.381.
Texto completoTesis sobre el tema "EGTA-AM"
Abate, Ilaria. "Chronic intracellular Ca2+ buffering shapes Ca2+ oscillations in developing spinal interneurons". Doctoral thesis, Università degli studi di Trieste, 2013. http://hdl.handle.net/10077/8546.
Texto completoDuring the development of spinal cord, the maturation of neuronal circuits is a complex process, involving genetic and epigenetic mechanisms cooperating for the maturation of motor control (Jessell, 2000; Kiehn, 2006). Variations in the concentration of intracellular Ca2+ are crucial signals in this process of maturation; in fact, Ca2+ signals may lead to the emergence of specific neuronal phenotypes or guide the formation of cellular connectivity. The organotypic cultures of embryonic mouse spinal cord represent an ideal experimental approach to study the maturation and physiology of the individual neurons and spinal networks. In fact, this experimental model reproduces in vitro the heterogeneous populations of cells, the three dimensional connections between these cells and the basic cytoarchitecture of the spinal cord observed in in vivo development (Avossa et al., 2003). In this experimental model, three different types of Ca2+ activity have been identified and characterized: waves, bursts and oscillations (Fabbro et al., 2007; Sibilla et al., 2009). These Ca2+ signals are all generated by ventral interneurons, but each of them shows a specific pattern of expression during development and has different underlying mechanisms. In this thesis, I focused my attention on the most peculiar of these Ca2+ signals: the electrical activity-independent Ca2+ oscillations. The main aim of my thesis was to better clarify the mechanisms underlying the generation and role of Ca2+ oscillations in spinal neurons, by investigating the effects of pharmacological manipulation of intracellular Ca2+ buffering on Ca2+ oscillations behavior, neuronal biophysical properties and neuronal network activity in organotypic spinal cultures. To this aim, I treated spinal cord slices with two different intracellular Ca2+ buffers, BAPTA-AM and EGTA-AM, and I monitored their impact using both Ca2+-imaging and single cell patch-clamp techniques. Initially, I investigated the effects on Ca2+ oscillations induced by both chronic and acute treatment with BAPTA-AM. For the first time I described a change in the activity of oscillating neurons. In particular, after chronic incubation with BAPTA-AM, I reported a significant increase in the number of neurons recruited to generate Ca2+ oscillations, which was accompanied by a modulation of oscillations kinetic. Ca2+ oscillations recorded after chronic incubation with BAPTA-AM maintained their peculiar features (Fabbro et al., 2007; Sibilla et al., 2009), in particular their Ca2+-dependence, thus supporting the idea that the BAPTA-induced oscillations represent an amplification of the true oscillations phenomena, amplified by a prolonged intracellular Ca2+ buffering. Despite a potentiating effect of chronic BAPTA-AM treatment on Ca2+ oscillations, its acute application completely blocked Ca2+ oscillations in all neurons. The next step was to verify whether the observed effects could be related to changes in the biophysical properties of neurons or in neuronal network electrical activity. By patch clamp experiments I showed that the chronic BAPTA-AM treatment induces a significant enhancement in the frequency of heterogeneous (GABA-glycine and AMPA mediated) spontaneous post-synaptic currents (PSCs) when compared to untreated cultures. Neuronal membrane capacitance and input resistance were comparable to those of control neurons, thus confirming neuronal health. As the reported results pointed to an increased excitability at the level of single neuron, I analyzed the impact of BAPTA treatment on the functional expression of a family of channels extremely important in the regulation of neuronal excitability: voltage-gated K+ channels. I observed the presence of a significant increase in the amplitude of K+ currents (IK) in slices chronically treated with BAPTA-AM. To analyze the type of IK involved I separated the different IK components (Ca2+-dependent -IK(Ca)- , transient -IK(A)- and delayed-rectifier -IK(DR)-), demonstrating that, in BAPTA-AM treated cultures, the IK(Ca) and IK(A) components were similar to control cultures. Conversely, I found a potentiation of IK(DR), i.e. an increase in its maximal current amplitude. Furthermore, I found that acute application of BAPTA-AM partially reduces the magnitude of total IK. Action potentials are other critical players reflecting neuronal excitability. Chronic BAPTA-AM treatment did not affect action potential kinetic; however, I found that BAPTA-treated neurons show a different distribution profile of excitability, with a widening of the population of ventral spinal interneurons displaying a tonic firing pattern and a decrease in the one showing an adapting firing behavior. To explore the specificity of BAPTA-AM effects I employed another intracellular Ca2+ chelator: EGTA-AM. I reported, as a consequence of a chronic EGTA-AM treatment of spinal neurons, an increase in the population of oscillating neurons (similarly to BAPTA treatment), but, without changes in oscillations kinetic. However, the study of synaptic activity in EGTA-AM treated slices did not reveal any change in the frequency or kinetic of spontaneous or miniature PSCs. Interestingly, in contrast to BAPTA treatment, EGTA-AM had no effect on IK. Overall, the results reported in this thesis show, on one hand, a specific effect of BAPTA-AM on K+; most importantly, on the other hand, they support the needing of a correct intracellular Ca2+ homeostasis for the genesis of Ca2+ oscillations and indicate the presence of a homeostatic adaptation as a rebound effect of chronic manipulation of intracellular Ca2+.
XXV Ciclo
1982
Actas de conferencias sobre el tema "EGTA-AM"
Davies, T. A., D. Drotts, G. Weil y E. R. Simons. "THROMBIN-INDUCED STIMULATION OF HUMAN PLATELETS LEADS TO AN INCREASE IN CYTOPLASMIC CALCIUM". En XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644471.
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