Extrusion of Ca2+ from Mouse Motor Terminal Mitochondria Via a Na+-ca2+ Exchanger Increases Post-tetanic Evoked Release.
From: Department of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, FL 33101, USA.
The Journal of physiology
- Publish Date: Aug 2006
- ISSN: 0022-3751
- Volume: 574
- Issue: Pt 3
- Pages: 663-75
- Medium: Print
- Language: English
- Citation (JAMA): García-Chacón Luis E, Nguyen Khanh T, David Gavriel, et al. Extrusion of Ca2+ from Mouse Motor Terminal Mitochondria Via a Na+-ca2+ Exchanger Increases Post-tetanic Evoked Release.. J. Physiol. (Lond.) Aug 2006;574:663-75
Abstract
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 microM) 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 microM) had no significant effect on the decay of mitochondrial [Ca2+]. Inhibition of the mitochondrial Na+-Ca2+ exchanger with CGP-37157 (50 microM) 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.
Mesh Headings (Keywords): Action Potentials, Animals, Calcium, Calcium Signaling, Cells, Cultured, Electric Stimulation, Mice, Mice, Inbred C57BL, Mitochondria, Motor Neurons, Muscle Contraction, Muscle, Skeletal, Presynaptic Terminals, Sodium-Calcium Exchanger
Check for Full Text / PubMed Unique Identifier (PMID): 16613870
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