Evidence for two separate purinergic responses in Paramecium tetraurelia: XTP inhibits only the oscillatory responses to GTP.

The purine nucleotide GTP causes a complex behavioral response and two distinct electrophysiological responses in the ciliated protozoan Paramecium tetraurelia. One of the two electrophysiological responses is an oscillating current that is responsible for the repeated backward swimming episodes that constitute the behavioral response to GTP. The second electrophysiological response is a sustained current whose relationship to the first is unknown. Here we show that the purine nucleotides XTP can completely block both the behavioral response to GTP and its associated oscillating current, but not the sustained current induced by GTP. Notably, XTP alone causes a sustained current similar to that induced by GTP. We believe the data support the notion that P. tetraurelia possesses two distinct signal transduction pathways sensitive to purine nucleotides: one specific for GTP that leads to oscillating currents and behavior, and a second pathway activated by GTP and other purine nucleotides that leads to a sustained current.

Oscillating response to a purine nucleotide disrupted by mutation in Paramecium tetraurelia.

The purine nucleotide GTP, when added extracellularly, induces oscillations in the swimming behaviour of the protist Paramecium tetraurelia. For periods as long as 10 min the cell swims backwards and forwards repetitively. The oscillations in swimming behaviour are driven by changes in membrane potential of the cell, which in turn are caused by periodic activation of inward Mg2+- and Na+-specific currents. We screened for and isolated mutants that are defective in this response, exploiting the fact that the net result of GTP on a population of cells is repulsion. One mutant, GTP-insensitive (gin A), is not repelled by GTP. In addition, GTP fails to induce repetitive backwards swimming in gin A mutants, although they swim backwards normally in response to other stimuli. GTP fails to evoke oscillations in membrane potential or Mg2+ and Na+ currents in the mutant, although the Mg2+ and Na+ conductances are not themselves measurably affected. A small, oscillating Ca2+ current induced by GTP in the wild type, which might be part of the mechanism that generates oscillations, is also missing from gin A cells. To our knowledge, gin A is the first example of a mutant defective in a purinergic response. We discuss the possibility that the gin A lesion affects the oscillator itself.