Correlation between loss of a Mg2+ conductance and an adaptation defect ina mutant of Paramecium tetraurelia

Paramecium tetraurelia responds to chronic KCl-induced depolarization by sw imming backward, but the ciliate recovers within seconds and then undergoes a prolonged adaptation period during which sensitivity to external stimuli is altered radically. We examined the role of Mg2+ in this phenomenon. pro mpted by finding that mutations in the eccentric-A gene both suppressed a M g2+-specific conductance and prevented adaptation. Adaptation of the wild t ype proceeded normally when extracellular Mg2+ was varied from 0-20 mM, how ever, suggesting that channel-mediated Mg2+ fluxes were not involved. In se eking alternative explanations for the eccentric mutant phenotype, we ascer tained that there was an osmotic component to adaptation but that K+-induce d depolarization was the primary stimulus. We also noted that wild-type and eccentric mutant cells depolarized by equivalent amounts in KCl, suggestin g that the genetic lesion must lie downstream of membrane-potential change. We also examined whether the adaptation-induced behavioral changes and, in deed, the defect in eccentric might be explained in terms of Mg2+ and Na+ e fflux during behavioral resting, but experimental observations failed to su pport this notion. Finally, we consider the possibility that eccentric gene mutation prevents adaptation by interfering with intracellular free Mg2+ h omeostasis in Paramecium.