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This Article Full Text Full Text (PDF) Supplemental Movies All Versions of this Article: 291/6/C1193    most recent 00230.2006v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Beltran-Parrazal, L. Articles by Charles, A. C. Search for Related Content PubMed PubMed Citation Articles by Beltran-Parrazal, L. Articles by Charles, A. C.

MITOCHONDRIAL MODELING AND FUNCTION

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

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