2024-03-28T21:18:14Zhttp://uvadoc.uva.es/oai/requestoai:uvadoc.uva.es:10324/218092021-06-23T09:52:12Zcom_10324_1134com_10324_931com_10324_894col_10324_1213
Calvo Rodríguez, María
García Durillo, Mónica
Villalobos Jorge, Carlos
Núñez Llorente, Lucía
2016-12-16T12:17:52Z
2016-12-16T12:17:52Z
2016
Biochim Biophys Acta Mol Cel Res 1863(11): 2637-2649
1388-1981
http://uvadoc.uva.es/handle/10324/21809
10.1016/j.bbamcr.2016.08.001
Aging is associated to cognitive decline and susceptibility to neuron death, two processes related recently to subcellular
Ca2+ homeostasis. Memory storage relies on mushroom spines stability that depends on store-operated
Ca2+ entry (SOCE). In addition, Ca2+ transfer from endoplasmic reticulum(ER) to mitochondria sustains energy
production but mitochondrial Ca2+ overload promotes apoptosis. We have addressed whether SOCE and ERmitochondria
Ca2+ transfer are influenced by culture time in long-term cultures of rat hippocampal neurons, a
model of neuronal aging.We found that short-term cultured neurons show large SOCE, low Ca2+ store content
and 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 is
enhanced, expression of the mitochondrial Ca2+ uniporter (MCU) increases and most Ca2+ released from the ER
is transferred to mitochondria. These results suggest that neuronal aging is associated to increased ERmitochondrial
cross talking and loss of SOCE. This subcellular Ca2+ remodeling might contribute to cognitive decline
and susceptibility to neuron cell death in the elderly.
eng
info:eu-repo/semantics/openAccess
http://creativecommons.org/licenses/by-nc-nd/4.0/
Attribution-NonCommercial-NoDerivatives 4.0 International
Hippocampal neurons
In vitro aging promotes endoplasmic reticulum (ER)-mitochondria Ca2+ cross talk and loss of store-operated Ca2+ entry (SOCE) in rat hippocampal neurons
info:eu-repo/semantics/article