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Difference between revisions of "Barksdale 2010 FASEB J"

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|year=2010
|year=2010
|journal=FASEB J
|journal=FASEB J
|abstract=Neuronal function in the brain requires energy in the form of ATP, and mitochondria are canonically associated with ATP production in neurons. The electrochemical gradient, which underlies the mitochondrial transmembrane potential (DeltaPsi(mt)), is harnessed for ATP generation. Here we show that DeltaPsi(mt) and ATP-production can be engaged in mitochondria isolated from human brains up to 8.5 h postmortem. Also, a time course of postmortem intervals from 0 to 24 h using mitochondria isolated from mouse cortex reveals that DeltaPsi(mt) in mitochondria can be reconstituted beyond 10 h postmortem. It was found that Complex I of the mitochondrial electron transport chain was affected adversely with increasing postmortem intervals. Mitochondria isolated from postmortem mouse brains maintain the ability to produce ATP, but rates of production decreased with longer postmortem intervals. Furthermore, we show that postmortem brain mitochondria retain their DeltaPsi(mt) and ATP-production capacities following cryopreservation. Our finding that DeltaPsi(mt) and ATP-generating capacity can be reinitiated in brain mitochondria hours after death indicates that human postmortem brains can be an abundant source of viable mitochondria to study metabolic processes in health and disease. It is also possible to archive these mitochondria for future studies.
|abstract=Neuronal function in the brain requires energy in the form of ATP, and mitochondria are canonically associated with ATP production in neurons. The electrochemical gradient, which underlies the mitochondrial transmembrane potential (ΔΨ<sub>mem</sub>), is harnessed for ATP generation. Here we show that ΔΨmem and ATP-production can be engaged in mitochondria isolated from human brains up to 8.5 h postmortem. Also, a time course of postmortem intervals from 0 to 24 h using mitochondria isolated from mouse cortex reveals that ΔΨmem in mitochondria can be reconstituted beyond 10 h postmortem. It was found that complex I of the mitochondrial electron transport chain was affected adversely with increasing postmortem intervals. Mitochondria isolated from postmortem mouse brains maintain the ability to produce ATP, but rates of production decreased with longer postmortem intervals. Furthermore, we show that postmortem brain mitochondria retain their ΔΨ<sub>mem</sub> and ATP-production capacities following cryopreservation. Our finding that ΔΨ<sub>mem</sub> and ATP-generating capacity can be reinitiated in brain mitochondria hours after death indicates that human postmortem brains can be an abundant source of viable mitochondria to study metabolic processes in health and disease. It is also possible to archive these mitochondria for future studies.
|keywords=ATP, Cortex, Electron microscopy, Membrane potential, Rhodamine
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Revision as of 12:02, 26 May 2015

Publications in the MiPMap
Barksdale KA, Perez-Costas E, Gandy JC, Melendez-Ferro M, Roberts RC, Bijur GN (2010) Mitochondrial viability in mouse and human postmortem brain. FASEB J 24:3590-9.

» PMID: 20466876 Open Access

Barksdale KA, Perez-Costas E, Gandy JC, Melendez-Ferro M, Roberts RC, Bijur GN (2010) FASEB J

Abstract: Neuronal function in the brain requires energy in the form of ATP, and mitochondria are canonically associated with ATP production in neurons. The electrochemical gradient, which underlies the mitochondrial transmembrane potential (ΔΨmem), is harnessed for ATP generation. Here we show that ΔΨmem and ATP-production can be engaged in mitochondria isolated from human brains up to 8.5 h postmortem. Also, a time course of postmortem intervals from 0 to 24 h using mitochondria isolated from mouse cortex reveals that ΔΨmem in mitochondria can be reconstituted beyond 10 h postmortem. It was found that complex I of the mitochondrial electron transport chain was affected adversely with increasing postmortem intervals. Mitochondria isolated from postmortem mouse brains maintain the ability to produce ATP, but rates of production decreased with longer postmortem intervals. Furthermore, we show that postmortem brain mitochondria retain their ΔΨmem and ATP-production capacities following cryopreservation. Our finding that ΔΨmem and ATP-generating capacity can be reinitiated in brain mitochondria hours after death indicates that human postmortem brains can be an abundant source of viable mitochondria to study metabolic processes in health and disease. It is also possible to archive these mitochondria for future studies. Keywords: ATP, Cortex, Electron microscopy, Membrane potential, Rhodamine


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Stress:Cryopreservation, Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property.  Organism: Human, Mouse  Tissue;cell: Nervous system  Preparation: Isolated mitochondria  Enzyme: Complex I  Regulation: ATP production, mt-Membrane potential