RT info:eu-repo/semantics/article
T1 Modulation of secretion by the endoplasmic reticulum in mouse chromaffin cells
A1 Rigual Bonastre, Ricardo Jaime
A1 Montero Zoccola, María Teresa
A1 Rico Martín, Alberto José
A1 Prieto Lloret, Jesús
A1 Alonso Alonso, María Teresa
A1 Álvarez Martín, Javier
K1 Retículo endoplasmático
K1 Células neuronales
AB The endoplasmic reticulum (ER) has been suggested to modulate secretion either behaving as a Ca2+ sink or as a Ca2+ sourcein neuronal cells. Working as a Ca2+ sink, through ER-Ca2+ pumping, it may reduce secretion induced by different stimuli.Instead, working as a Ca2+ source through the Ca2+ induced Ca2+ release (CICR) phenomenon, it may potentiate secretiontriggered by activation of plasma membrane Ca2+ channels. We have previously demonstrated the presence of CICR in bovinechromaffin cells, but we now find that mouse chromaffin cells almost lack functional caffeine-sensitive ryanodine receptors in theER and, consistently, no CICR from the ER could be observed. In addition, inhibition of ER Ca2+ pumping with ciclopiazonic acidor thapsigargin strongly stimulated high-K+-evoked catecholamine secretion and cytosolic [Ca2+] ([Ca2+]c) transients. Surprisingly,5 mM caffeine reduced high-K+-induced [Ca2+]c peaks but considerably potentiated secretion induced by high-K+ stimulation.However, this potentiation was insensitive to ryanodine and additive to that induced by emptying the ER of Ca2+ withthapsigargin, suggesting that it is unrelated to the activation of ryanodine receptors. We conclude that, in mouse chromaffin cells,CICR is not functional and the ER strongly inhibits secretion by acting as a damper of the [Ca2+]c signal.
PB Wiley
SN 0953-816X
YR 2002
FD 2002
LK http://uvadoc.uva.es/handle/10324/5996
UL http://uvadoc.uva.es/handle/10324/5996
LA eng
NO European Journal of Neuroscience, 2002, vol. 16, p. 1-8
NO Producción Científica
DS UVaDOC
RD 16-abr-2024