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<dc:title>Calcium signalling mediated through a7 and non-a7 nAChR stimulation is differentially regulated in bovine chromaffin cells to induce catecholamine release</dc:title>
<dc:creator>Barrio, Laura del</dc:creator>
<dc:creator>Egea, Javier</dc:creator>
<dc:creator>León, Rafael</dc:creator>
<dc:creator>Romero, Alejandro</dc:creator>
<dc:creator>Ruiz, Ana</dc:creator>
<dc:creator>Montero Zoccola, María Teresa</dc:creator>
<dc:creator>Álvarez Martín, Javier</dc:creator>
<dc:creator>López, Manuela G.</dc:creator>
<dc:subject>Calcio</dc:subject>
<dc:description>Producción Científica</dc:description>
<dc:description>Ca2+ signalling and exocytosis mediated by nicotinic receptor (nAChR) subtypes, especially the a7 nAChR, in bovine&#xd;
chromaffin cells are still matters of debate.We have used chromaffin cell cultures loaded with Fluo-4 or transfected with aequorins directed to the cytosol or&#xd;
mitochondria, several nAChR agonists (nicotine, 5-iodo-A-85380, PNU282987 and choline), and the a7 nAChR allosteric&#xd;
modulator PNU120596. Minimal [Ca2+]c transients, induced by low concentrations of selective a7 nAChR agonists and nicotine, were markedly&#xd;
increased by the a7 nAChR allosteric modulator PNU120596. These potentiated responses were completely blocked by the&#xd;
a7 nAChR antagonist a-bungarotoxin (a7-modulated-response). Conversely, high concentrations of the a7 nAChR agonists,&#xd;
nicotine or 5-iodo-A-85380 induced larger [Ca2+]c transients, that were blocked by mecamylamine but were unaffected by&#xd;
a-bungarotoxin (non-a7 response). [Ca2+]c increases mediated by a7 nAChR were related to Ca2+ entry through non-L-type&#xd;
Ca2+ channels, whereas non-a7 nAChR-mediated signals were related to L-type Ca2+ channels; Ca2+-induced Ca2+-release&#xd;
contributed to both responses. Mitochondrial involvement in the control of [Ca2+]c transients, mediated by either receptor,&#xd;
was minimal. Catecholamine release coupled to a7 nAChRs was more efficient in terms of catecholamine released/[Ca2+]c.</dc:description>
<dc:date>2014-09-16T16:37:02Z</dc:date>
<dc:date>2015-09-16T23:40:10Z</dc:date>
<dc:date>2011</dc:date>
<dc:type>info:eu-repo/semantics/article</dc:type>
<dc:identifier>British Journal of Pharmacology, 2011, vol. 162, p. 94-110</dc:identifier>
<dc:identifier>0007-1188</dc:identifier>
<dc:identifier>http://uvadoc.uva.es/handle/10324/5995</dc:identifier>
<dc:identifier>10.1111/j.1476-5381.2010.01034.x</dc:identifier>
<dc:identifier>94</dc:identifier>
<dc:identifier>110</dc:identifier>
<dc:identifier>British Journal of Pharmacology</dc:identifier>
<dc:identifier>162</dc:identifier>
<dc:language>eng</dc:language>
<dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
<dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
<dc:rights>Attribution-NonCommercial-NoDerivatives 4.0 International</dc:rights>
<dc:publisher>Wiley</dc:publisher>
<dc:peerreviewed>SI</dc:peerreviewed>
</ow:Publication>
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