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Evidence that mitochondria buffer physiological Ca 2+ loads in lizard motor nerve terminals
Author(s) -
David Gavriel,
Barrett John N.,
Barrett Ellen F.
Publication year - 1998
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1111/j.1469-7793.1998.059bo.x
Subject(s) - cytosol , biophysics , mitochondrion , membrane potential , stimulation , chemistry , calcium , biochemistry , biology , endocrinology , organic chemistry , enzyme
1 Changes in cytosolic and mitochondrial [Ca 2+ ] produced by brief trains of action potentials were measured in motor nerve terminals using a rapidly scanning confocal microscope. Cytosolic [Ca 2+ ] was measured using ionophoretically injected Oregon Green BAPTA 5N (OG‐5N). Mitochondrial [Ca 2+ ] was measured using rhod‐2, bath loaded as dihydrorhod‐2. 2 In response to 100‐250 stimuli at 25‐100 Hz the average cytosolic [Ca 2+ ] showed an initial rapid increase followed by a much slower rate of increase. Mitochondrial [Ca 2+ ] showed no detectable increase during the first fifteen to twenty stimuli, but after this initial delay also showed an initially rapid rise followed by a slower rate of increase. The onset of the increase in mitochondrial [Ca 2+ ] coincided with the slowing of the rate of rise of cytosolic [Ca 2+ ]. The peak levels of cytosolic and mitochondrial [Ca 2+ ] both increased with increasing frequencies of stimulation. 3 When stimulation terminated, the initial rate of decay of cytosolic [Ca 2+ ] was much more rapid than that of mitochondrial [Ca 2+ ]. 4 After addition of carbonyl cyanide m‐chlorophenyl hydrazone (CCCP, 1‐2 μ m ) to dissipate the proton electrochemical gradient across the mitochondrial membrane, cytosolic [Ca 2+ ] rose rapidly throughout the stimulus train, reaching levels much higher than normal. CCCP inhibited the increase in mitochondrial [Ca 2+ ]. 5 These results suggest that mitochondrial uptake of Ca 2+ contributes importantly to buffering presynaptic cytosolic [Ca 2+ ] during normal neuromuscular transmission.