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¹ Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, PO Box 016430, Miami, FL 33101, USA

To investigate mitochondrial responses to repetitive stimulation, we measured changes in NADH fluorescence and mitochondrial membrane potential (_m) produced by trains of action potentials (50 Hz for 10–50 s) delivered to motor nerve terminals innervating external intercostal muscles. Stimulation produced a rapid decrease in NADH fluorescence and partial depolarization of _m. These changes were blocked when Ca²⁺ was removed from the bath or when N-type Ca²⁺ channels were inhibited with -conotoxin GVIA, but were not blocked when bath Ca²⁺ was replaced by Sr²⁺, or when vesicular release was inhibited with botulinum toxin A. When stimulation stopped, NADH fluorescence and _m returned to baseline values much faster than mitochondrial [Ca²⁺]. In contrast to findings in other tissues, there was usually little or no poststimulation overshoot of NADH fluorescence. These findings suggest that the major change in motor terminal mitochondrial function brought about by repetitive stimulation is a rapid acceleration of electron transport chain (ETC) activity due to the _m depolarization produced by mitochondrial Ca²⁺ (or Sr²⁺) influx. After partial inhibition of complex I of the ETC with amytal, stimulation produced greater _m depolarization and a greater elevation of cytosolic [Ca²⁺]. These results suggest that the ability to accelerate ETC activity is important for normal mitochondrial sequestration of stimulation-induced Ca²⁺ loads.

(Received 11 December 2006; accepted after revision 26 December 2006; first published online 4 January 2007)
Corresponding author G. David: Department of Physiology and Biophysics, Miller School of Medicine, University of Miami, PO Box 016430, Miami, FL 33101, USA. Email: gdavid{at}med.miami.edu

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