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oai: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 Hippocampal neurons Producción Científica 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. 2016-12-16 2016-12-16 2016 info:eu-repo/semantics/article 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 eng http://www.journals.elsevier.com/bba-molecular-and-cell-biology-of-lipids/ info:eu-repo/semantics/openAccess http://creativecommons.org/licenses/by-nc-nd/4.0/ Attribution-NonCommercial-NoDerivatives 4.0 International Elsevier