RT info:eu-repo/semantics/article
T1 Calcium signalling mediated through a7 and non-a7 nAChR stimulation is differentially regulated in bovine chromaffin cells to induce catecholamine release
A1 Barrio, Laura del
A1 Egea, Javier
A1 León, Rafael
A1 Romero, Alejandro
A1 Ruiz, Ana
A1 Montero Zoccola, María Teresa
A1 Álvarez Martín, Javier
A1 López, Manuela G.
K1 Calcio
AB Ca2+ signalling and exocytosis mediated by nicotinic receptor (nAChR) subtypes, especially the a7 nAChR, in bovinechromaffin cells are still matters of debate.We have used chromaffin cell cultures loaded with Fluo-4 or transfected with aequorins directed to the cytosol ormitochondria, several nAChR agonists (nicotine, 5-iodo-A-85380, PNU282987 and choline), and the a7 nAChR allostericmodulator PNU120596. Minimal [Ca2+]c transients, induced by low concentrations of selective a7 nAChR agonists and nicotine, were markedlyincreased by the a7 nAChR allosteric modulator PNU120596. These potentiated responses were completely blocked by thea7 nAChR antagonist a-bungarotoxin (a7-modulated-response). Conversely, high concentrations of the a7 nAChR agonists,nicotine or 5-iodo-A-85380 induced larger [Ca2+]c transients, that were blocked by mecamylamine but were unaffected bya-bungarotoxin (non-a7 response). [Ca2+]c increases mediated by a7 nAChR were related to Ca2+ entry through non-L-typeCa2+ channels, whereas non-a7 nAChR-mediated signals were related to L-type Ca2+ channels; Ca2+-induced Ca2+-releasecontributed to both responses. Mitochondrial involvement in the control of [Ca2+]c transients, mediated by either receptor,was minimal. Catecholamine release coupled to a7 nAChRs was more efficient in terms of catecholamine released/[Ca2+]c.
PB Wiley
SN 0007-1188
YR 2011
FD 2011
LK http://uvadoc.uva.es/handle/10324/5995
UL http://uvadoc.uva.es/handle/10324/5995
LA eng
NO British Journal of Pharmacology, 2011, vol. 162, p. 94-110
NO Producción Científica
DS UVaDOC
RD 22-nov-2024