Electrical stimulation of the mammalian neurohypophysial infundibular stalk evokes the entry of Nat and Ca2t into the neurosecretory terminals during the action potential. These events, in turn, increase intracellular Ca2t and activate NaK- and Ca-ATPases, prompting the mitochondria to increase oxidative phosphorylation which can be monitored by recording the changes in FAD and NADH fluorescence. This paper reflects our efforts to determine whether or not modulating the capacity of mitochondria to produce ATP, by changing the concentrations of two important substrates of the Krebs cycle of the nerve terminal mitochondria, pyruvate and glucose, has an effect on the intrinsic fluorescence changes triggered by action potential stimulation.