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1 Physiology and Biophysics, Univ. of Miami Sch. of Medicine, Miami, FL, USA
* To whom correspondence should be addressed. E-mail: ebarrett2{at}med.miami.edu.
We investigated how inhibition of mitochondrial Ca2+ uptake affects stimulation-induced increases in cytosolic [Ca2+], and phasic and asynchronous transmitter release, in lizard motor terminals in 2 and 0.5 mM bath [Ca2+]. Lowering bath [Ca2+] reduced the rate of rise, but not the final amplitude, of the increase in mitochondrial [Ca2+] during 50 Hz stimulation. The amplitude of the stimulation-induced increase in cytosolic [Ca2+] was reduced in low bath [Ca2+], and increased when mitochondrial Ca2+ uptake was inhibited by depolarizing mitochondria. In 2 mM Ca2+ end-plate potentials (epps) depressed by 53% following 10 s of 50 Hz stimulation, and this depression increased to 80% following mitochondrial depolarization. In contrast, in 0.5 mM Ca2+ the same stimulation pattern increased epps by about 3.4-fold, and this increase was even greater (transiently) following mitochondrial depolarization. In both 2 and 0.5 mM [Ca2+] mitochondrial depolarization increased asynchronous release during the 50 Hz train, and increased the total vesicular release (phasic and asynchronous) measured by destaining of the styryl dye FM2-10. These results suggest that, by limiting the stimulation-induced increase in cytosolic [Ca2+], mitochondrial Ca2+ uptake maintains a high ratio of phasic to asynchronous release, thus helping to sustain neuromuscular transmission during repetitive stimulation. Interestingly, the quantal content of the epp reached during 50 Hz stimulation stabilized at a similar level (~20 quanta) in both 2 and 0.5 mM Ca2+. A similar convergence was measured in oligomycin, which inhibits mitochondrial ATP synthesis without depolarizing mitochondria, but quantal contents fell below 20 when mitochondria were depolarized in 2 mM Ca2+.
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