Paramecium aurelia and its behavioral mutants are used as a model system for excitable membranes such as nerves and muscles. The ciliate membrane exhibits a voltage-dependent increase in calcium conductance which accompanies ciliary reversal. Pawn mutants do not exhibit the same electrical changes in the membranes as do wild type cells and they also are different in that they cannot swim backward. Influx of Ca 2 ion following depolarization is believed to increase intracellular (intraciliary) Ca 2 ion concentrations above a threshold which controls the ciliary beat effective stroke (calcium current hypothesis). Alternatively, Ca 2 ion may exert its effect on beat orientation by being displaced or removed from sites near or at the surface membrane (cation exchange hypothesis). This project emphasizes biochemical studies to better understand membrane gating mechanisms to cations, and ciliary beat orientation. Detailed analyses of lipids and proteins from various wild type and mutant strains are being conducted. In addition, ultrastructural studies using cytochemical methods, and the use of compounds which alter membrane permeabilities and their effects on cilia behavior are also in progress. BIBLIOGRAPHIC REFERENCES: Fisher, G. W. and E. S. Kaneshiro. 1975. Ultra structural localization of calcium deposits in cilia of Paramecium aurelia. J. Cell Biol. 67: 115a. Fisher, G. W., E. S. Kaneshiro and P. D. Peters. 1976. Divalent cation affinity sites in Paramecium aurelia. J. Cell Biol. (In Press).