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Статті в журналах з теми "BAPTA-AM"
Pastorino, J. G., J. W. Snyder, J. B. Hoek, and J. L. Farber. "Ca2+ depletion prevents anoxic death of hepatocytes by inhibiting mitochondrial permeability transition." American Journal of Physiology-Cell Physiology 268, no. 3 (March 1, 1995): C676—C685. http://dx.doi.org/10.1152/ajpcell.1995.268.3.c676.
Повний текст джерелаKuijpers, T. W., M. Hoogerwerf, and D. Roos. "Neutrophil migration across monolayers of resting or cytokine-activated endothelial cells. Role of intracellular calcium changes and fusion of specific granules with the plasma membrane." Journal of Immunology 148, no. 1 (January 1, 1992): 72–77. http://dx.doi.org/10.4049/jimmunol.148.1.72.
Повний текст джерелаBillman, G. E. "Intracellular calcium chelator, BAPTA-AM, prevents cocaine-induced ventricular fibrillation." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 5 (November 1, 1993): H1529—H1535. http://dx.doi.org/10.1152/ajpheart.1993.265.5.h1529.
Повний текст джерелаTymianski, Michael, Igor Spigelman, Liang Zhang, Peter L. Carlen, Charles H. Tator, Milton P. Charlton, and M. Christopher Wallace. "Mechanism of Action and Persistence of Neuroprotection by Cell-Permeant Ca2+ Chelators." Journal of Cerebral Blood Flow & Metabolism 14, no. 6 (November 1994): 911–23. http://dx.doi.org/10.1038/jcbfm.1994.122.
Повний текст джерелаLiu, Qing, Ulrike Möller, Daniela Flügel, and Thomas Kietzmann. "Induction of plasminogen activator inhibitor I gene expression by intracellular calcium via hypoxia-inducible factor-1." Blood 104, no. 13 (December 15, 2004): 3993–4001. http://dx.doi.org/10.1182/blood-2004-03-1017.
Повний текст джерелаCui, Xiao-Lan, Wen-Wu Jin, Ya-Xian Ding, Larry D. Alexander, Ulrich Hopfer, and Janice G. Douglas. "Ca2+-dependent activation of c-junNH2-terminal kinase in primary rabbit proximal tubule epithelial cells." American Journal of Physiology-Cell Physiology 279, no. 2 (August 1, 2000): C403—C409. http://dx.doi.org/10.1152/ajpcell.2000.279.2.c403.
Повний текст джерелаTymianski, M., M. P. Charlton, P. L. Carlen, and C. H. Tator. "Properties of neuroprotective cell-permeant Ca2+ chelators: effects on [Ca2+]i and glutamate neurotoxicity in vitro." Journal of Neurophysiology 72, no. 4 (October 1, 1994): 1973–92. http://dx.doi.org/10.1152/jn.1994.72.4.1973.
Повний текст джерелаMaloney, Judith A., Oxana M. Tsygankova, Lijun Yang, Qiuyang Li, Agnieszka Szot, Kemal Baysal, and John R. Williamson. "Activation of ERK by Ca2+store depletion in rat liver epithelial cells." American Journal of Physiology-Cell Physiology 276, no. 1 (January 1, 1999): C221—C230. http://dx.doi.org/10.1152/ajpcell.1999.276.1.c221.
Повний текст джерелаHorváth, Balázs, Bence Hegyi, Kornél Kistamás, Krisztina Váczi, Tamás Bányász, János Magyar, Norbert Szentandrássy, and Péter P. Nánási. "Cytosolic calcium changes affect the incidence of early afterdepolarizations in canine ventricular myocytes." Canadian Journal of Physiology and Pharmacology 93, no. 7 (July 2015): 527–34. http://dx.doi.org/10.1139/cjpp-2014-0511.
Повний текст джерелаMiteva, Anna, Alexander Gaydukov, and Olga Balezina. "Interaction between Calcium Chelators and the Activity of P2X7 Receptors in Mouse Motor Synapses." International Journal of Molecular Sciences 21, no. 6 (March 16, 2020): 2034. http://dx.doi.org/10.3390/ijms21062034.
Повний текст джерелаДисертації з теми "BAPTA-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.
Повний текст джерелаDuring 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
Книги з теми "BAPTA-AM"
Sade, Shachar. The pharmacokinetics and neuroprotective efficacy of BAPTA-AM in the rat following intraperitoneal injection. Ottawa: National Library of Canada, 1996.
Знайти повний текст джерелаТези доповідей конференцій з теми "BAPTA-AM"
Davies, T. A., D. Drotts, G. Weil, and E. R. Simons. "THROMBIN-INDUCED STIMULATION OF HUMAN PLATELETS LEADS TO AN INCREASE IN CYTOPLASMIC CALCIUM." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644471.
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