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Am J Physiol Cell Physiol (August 2, 2006). doi:10.1152/ajpcell.00230.2006
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Submitted on May 1, 2006
Accepted on July 24, 2006

Mitochondrial transport in processes of cortical neurons is independent of intracellular calcium.

Luis Beltran-Parrazal1, Hector Lopez-Valdez2, Kevin C Brennan1, Mauricio Diaz-Munoz3, Jean de Vellis4, and Andrew C Charles1*

1 Neurology, UCLA, Los angeles, California, United States
2 Neurology, UCLA, Los Angeles, California, United States
3 Molecular Neurobiology, Neurobiology Institute, Querétaro, Mexico
4 Mental Retardation Research Center, UCLA, Los ANgeles, California, United States

* To whom correspondence should be addressed. E-mail: acharles{at}ucla.ucla.

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 [Ca2+]i in rat cortical neurons. A significant percentage (27 %) of the total mitochondrial in cortical neuronal processes showed movement over distances of > 2 µM. The average velocity was 0.52 µm/sec. 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 (1µM) 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.




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