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Stimulation produced a rapid decrease in NADH fluorescence and partial depolarization of \u03a8<jats:sub>m<\/jats:sub>. These changes were blocked when Ca<jats:sup>2+<\/jats:sup> was removed from the bath or when N\u2010type Ca<jats:sup>2+<\/jats:sup> channels were inhibited with \u03c9\u2010conotoxin GVIA, but were not blocked when bath Ca<jats:sup>2+<\/jats:sup> was replaced by Sr<jats:sup>2+<\/jats:sup>, or when vesicular release was inhibited with botulinum toxin A. When stimulation stopped, NADH fluorescence and \u03a8<jats:sub>m<\/jats:sub> returned to baseline values much faster than mitochondrial [Ca<jats:sup>2+<\/jats:sup>]. 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 \u03a8<jats:sub>m<\/jats:sub> depolarization produced by mitochondrial Ca<jats:sup>2+<\/jats:sup> (or Sr<jats:sup>2+<\/jats:sup>) influx. After partial inhibition of complex I of the ETC with amytal, stimulation produced greater \u03a8<jats:sub>m<\/jats:sub> depolarization and a greater elevation of cytosolic [Ca<jats:sup>2+<\/jats:sup>]. These results suggest that the ability to accelerate ETC activity is important for normal mitochondrial sequestration of stimulation\u2010induced Ca<jats:sup>2+<\/jats:sup> loads.<\/jats:p>","DOI":"10.1113\/jphysiol.2006.126383","type":"journal-article","created":{"date-parts":[[2007,1,12]],"date-time":"2007-01-12T01:25:13Z","timestamp":1168565113000},"page":"783-798","source":"Crossref","is-referenced-by-count":34,"title":["Stimulation\u2010induced changes in NADH fluorescence and mitochondrial membrane potential in lizard motor nerve terminals"],"prefix":"10.1113","volume":"579","author":[{"given":"Janet","family":"Talbot","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John N.","family":"Barrett","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ellen 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