RT info:eu-repo/semantics/article
T1 In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2+ cross talk and loss of store-operated Ca2+ entry (SOCE) in rat hippocampal neurons
A1 Calvo Rodríguez, María
A1 García Durillo, Mónica
A1 Villalobos Jorge, Carlos
A1 Núñez Llorente, Lucía
K1 Hippocampal neurons
AB Aging is associated to cognitive decline and susceptibility to neuron death, two processes related recently to subcellularCa2+ homeostasis. Memory storage relies on mushroom spines stability that depends on store-operatedCa2+ entry (SOCE). In addition, Ca2+ transfer from endoplasmic reticulum(ER) to mitochondria sustains energyproduction but mitochondrial Ca2+ overload promotes apoptosis. We have addressed whether SOCE and ERmitochondriaCa2+ transfer are influenced by culture time in long-term cultures of rat hippocampal neurons, amodel of neuronal aging.We found that short-term cultured neurons show large SOCE, low Ca2+ store contentand no functional coupling between ER and mitochondria. In contrast, in long-term cultures reflecting aging neurons,SOCE is essentially lost, Stim1 and Orai1 are downregulated, Ca2+ stores becomeoverloaded, Ca2+ release isenhanced, expression of the mitochondrial Ca2+ uniporter (MCU) increases and most Ca2+ released from the ERis transferred to mitochondria. These results suggest that neuronal aging is associated to increased ERmitochondrialcross talking and loss of SOCE. This subcellular Ca2+ remodeling might contribute to cognitive declineand susceptibility to neuron cell death in the elderly.
PB Elsevier
SN 1388-1981
YR 2016
FD 2016
LK http://uvadoc.uva.es/handle/10324/21809
UL http://uvadoc.uva.es/handle/10324/21809
LA eng
NO Biochim Biophys Acta Mol Cel Res 1863(11): 2637-2649
NO Producción Científica
DS UVaDOC
RD 01-may-2024