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MITOCHONDRIAL MODELING AND FUNCTION
1Department of Neurology, David Geffen School of Medicine and 2Mental Retardation Research Center, University of California at Los Angeles, Los Angeles, California; 3Department of Cellular and Molecular Neurobiology, Universidad Nacional Autónoma de México-Juriquilla, Querétaro, México
Submitted 1 May 2006 ; accepted in final form 24 July 2006
Mitochondria show extensive movement along neuronal processes, but the mechanisms and function of this movement are not clearly understood. We have used high-resolution confocal microscopy to simultaneously monitor movement of mitochondria and changes in intracellular [Ca2+] ([Ca2+]i) in rat cortical neurons. A significant percentage (27%) of the total mitochondria in cortical neuronal processes showed movement over distances of >2 µM. The average velocity was 0.52 µm/s. The velocity, direction, and pattern of mitochondrial movement were not affected by transient increases in [Ca2+]i associated with spontaneous firing of action potentials. Stimulation of Ca2+ transients with forskolin (10 µM) or bicuculline (10 µM), or sustained elevations of [Ca2+]i evoked by glutamate (10 µM) also had no effect on mitochondrial transit. Neither removal of extracellular Ca2+, depletion of intracellular Ca2+ stores with thapsigargin, or inhibition of synaptic activity with TTX (1 µM) or a cocktail of CNQX (10 µM) and MK801 (10 µM) affected mitochondrial movement. These results indicate that movement of mitochondria along processes is a fundamental activity in neurons that occurs independently of physiological changes in [Ca2+]i associated with action potential firing, synaptic activity, or release of Ca2+ from intracellular stores.
calcium transient; dendrites
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