Significant Differences Between Procyclic and Bloodstream Forms of Trypanosoma brucei in the Maintenance of their Plasma Membrane Potential

The plasma membrane potential (ΔΨ) of procyclic and bloodstream trypomastigotes of Trypanosoma brucei was studied using the potentiometric fluorescent dye bisoxonol. Our results suggest that a proton pump plays a significant role in the regulation of AΨ in procyclic and bloodstream forms, as evidenced by depolarization of the plasma membrane by H + ‐ATPase inhibitors (e.g. dicyclohexylcarbo‐diimide, N ‐ethylmaleimide, diethylstilbestrol, and bafilomycin A 1 ). In bloodstream stages the plasma membrane was significantly depolarized by ouabain only when the cells were incubated in sodium‐rich buffers indicating that a sodium pump was being inhibited. In contrast, ouabain had no effect on the AΨ of the procyclic stages in a sodium‐rich buffer. However, it induced an additional significant depolarization in these stages when their plasma membrane was already partially depolarized by the H + ‐ATPase inhibitor dicyclohexylcarbo‐diimide, indicating the presence of an ouabain‐sensitive sodium pump whose activity is masked by the H + ‐ATPase. Unlike procyclic forms, the AΨ of bloodstream‐stage trypomastigotes was markedly sensitive to extracellular Na + and K + concentrations. Thus, there are significant differences between procyclic and blooodstream forms in the maintenance of the AΨ and in their permeability to cations.