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• W2068504986 startingPage "124" @default.
• W2068504986 abstract "Activation of NMDA receptors produces large increases in cytosolic Ca2+ that are taken up into mitochondria. We used recombinant aequorin targeted to mitochondria to report changes in matrix Ca2+ in rat hippocampal neurons in culture. Upon binding Ca2+, aequorin emits a photon in a one-shot reaction that consumes the indicator. Here we show that stimulation with NMDA produced a mitochondrial Ca2+ response that rapidly inactivated. However, following a 30-min recovery period the response was restored, suggesting the presence of a pool of indicator that was not exposed to high Ca2+ during the initial stimulus. We speculate that aequorin distant from the Ca2+ source was protected from microdomains of high Ca2+ near the plasmalemma and that this aequorin moved, either by movement of individual mitochondria or via the mitochondrial tubular network, to replenish consumed indicator during the recovery time. A large Ca2+ increase in a subset of mitochondria could produce local changes in energy metabolism, regional Ca2+ buffering, and foci that initiate neurotoxic processes." @default.
• W2068504986 created "2016-06-24" @default.
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• W2068504986 date "2003-12-01" @default.
• W2068504986 modified "2023-10-11" @default.
• W2068504986 title "NMDA-evoked consumption and recovery of mitochondrially targeted aequorin suggests increased Ca2+ uptake by a subset of mitochondria in hippocampal neurons" @default.
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• W2068504986 doi "https://doi.org/10.1016/j.brainres.2003.09.022" @default.
• W2068504986 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/14642837" @default.
• W2068504986 hasPublicationYear "2003" @default.
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