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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 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