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This Article Full Text Full Text (PDF) All Versions of this Article: 574/3/663    most recent jphysiol.2006.110841v1 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 HighWire Citing Articles via Google Scholar Google Scholar Articles by García-Chacón, L. E. Articles by Barrett, E. F. Search for Related Content PubMed PubMed Citation Articles by García-Chacón, L. E. Articles by Barrett, E. F. Related Collections Neuroscience

¹ Department of Physiology and Biophysics
² Neuroscience Program, University of Miami Miller School of Medicine, Miami, FL 33101, USA

Mitochondria sequester much of the Ca²⁺ that enters motor nerve terminals during repetitive stimulation at frequencies exceeding 10–20 Hz. We studied the post-stimulation extrusion of Ca²⁺ from mitochondria by measuring changes in matrix [Ca²⁺] with fluorescent indicators loaded into motor terminal mitochondria in the mouse levator auris longus muscle. Trains of action potentials at 50 Hz produced a rapid increase in mitochondrial [Ca²⁺] followed by a plateau, which was usually maintained after the end of the stimulus train and then slowly decayed back to baseline. Increasing the Ca²⁺ load delivered to the terminal by increasing the number of stimuli (from 500 to 2000) or the stimulation frequency (from 50 to 100 Hz), by increasing bath [Ca²⁺], or by prolonging the action potential with 3,4-diaminopyridine (100 µM) prolonged the post-stimulation decay of mitochondrial [Ca²⁺] without increasing the amplitude of the plateau during stimulation. Inhibiting the opening of the mitochondrial permeability transition pore with cyclosporin A (5 µM) had no significant effect on the decay of mitochondrial [Ca²⁺]. Inhibition of the mitochondrial Na⁺–Ca²⁺ exchanger with CGP-37157 (50 µM) dramatically prolonged the post-stimulation decay of mitochondrial [Ca²⁺], reduced post-stimulation residual cytosolic [Ca²⁺], and reduced the amplitude of endplate potentials evoked after the end of a stimulus train in the presence of both low and normal bath [Ca²⁺]. These findings suggest that Ca²⁺ extrusion from motor terminal mitochondria occurs primarily via the mitochondrial Na⁺–Ca²⁺ exchanger and helps to sustain post-tetanic transmitter release at mouse neuromuscular junctions.

(Received 3 April 2006; accepted after revision 10 April 2006; first published online 13 April 2006)
Corresponding author E. F. Barrett: Department of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, FL 33101, USA. Email: ebarrett2{at}med.miami.edu

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