RT info:eu-repo/semantics/article
T1 Mitochondria and chromaffin cell function
A1 García-Sancho Martín, Francisco Javier
A1 Diego, Antonio M. G. de
A1 García, Antonio G.
K1 Nervioso, Sistema - Enfermedades
K1 Fisiología
AB Chromaffin cells are an excellent model for stimulus–secretion coupling. Ca2+ entry through plasma membranevoltage-operated Ca2+ channels (VOCC) is the triggerfor secretion, but the intracellular organelles contribute subtlenuances to the Ca2+ signal. The endoplasmic reticulumamplifies the cytosolic Ca2+ ([Ca2+]C) signal by Ca2+-induced Ca2+ release (CICR) and helps generation of microdomainswith high [Ca2+]C (HCMD) at the subplasmalemmalregion. These HCMD induce exocytosis of the dockedsecretory vesicles. Mitochondria close to VOCC take uplarge amounts of Ca2+ from HCMD and stop progressionof the Ca2+ wave towards the cell core. On the other hand,the increase of [Ca2+] at the mitochondrial matrix stimulatesrespiration and tunes energy production to the increasedneeds of the exocytic activity. At the end of stimulation,[Ca2+]C decreases rapidly and mitochondria release the Ca2+accumulated in the matrix through the Na+/Ca2+ exchanger.VOCC, CICR sites and nearby mitochondria form functionaltriads that co-localize at the subplasmalemmal area, wheresecretory vesicles wait ready for exocytosis. These triadsoptimize stimulus–secretion coupling while avoidingpropagation of the Ca2+ signal to the cell core. Perturbationof their functioning in neurons may contribute to the genesisof excitotoxicity, ageing mental retardation and/or neurodegenerativedisorders.
PB Springer-Verlag
SN 0031-6768
YR 2012
FD 2012
LK http://uvadoc.uva.es/handle/10324/6341
UL http://uvadoc.uva.es/handle/10324/6341
LA eng
NO Pflügers Archiv European Journal of Physiology, 2012, vol. 464, p. 33-41
NO Producción Científica
DS UVaDOC
RD 27-abr-2024