Mitochondria have long been recognized as the primary energy conversion organelle in Eukaryotic cells. More recent studies have illuminated other critical processes in cellular development that involve mitochondria, specifically roles in programmed cell death and cell division. Ciliates have a long history of contributing to our understanding of cellular processes including chemosensory behavior, genetic reorganization, calcium regulation, and ciliary function. Little work has been done on assessing the role of mitochondria in the cellular dynamics of Ciliates. Paramecium are excitable cells whose swimming behavior is regulated by membrane potential. Backward swimming responses can be initiated by depolarizing the cell with an increase in external K+ added to the bathing solution. We have identified a ryanodine-sensitive calcium flux in Paramecium that can be observed under such depolarizing conditions. When Paramecium were treated with ryanodine receptor antagonists, backward swimming responses initiated by K+ depolarization were significantly reduced, but not eliminated. Our attempts to localize these channels led not to the endoplasmic reticulum (the expected site of ryanodine receptor/channels) but to mitochondria. Increasing evidence suggests that ryanodine sensitive channels can be found in mitochondria. In addition, recent sequence analysis of the Paramecium genome reveals several channels with conserved ryanodine domains, although none with significant overall homology. Since Ca2+ is a mediator of the backward swimming response, we used the mitochondrial calcium-sensitive dye Rhod-2 to assess mitochondrial calcium contributions to depolarization. During a K+ – induced depolarization, Rhod-2 fluorescence in the mitochondria decreased by approximately 30%. When cells were treated with the ryanodine receptor antagonist dantrolene prior to depolarization, the loss of calcium from mitochondria was significantly attenuated. We conclude that mitochondrial calcium stores can extend backward swimming responses in Paramecium. We have also utilized MitoTracker dyes to observe mitochondrial phenotypes displayed during autogamy and autophagy in Paramecium. Disruption of mitochondrial outer membrane proteins result in increased autophagy and disruption of cell division in Paramecium.