Mutual contact of murine erythroleukemia cells activates depolarizing cation channels, whereas contact with extracellular substrata activates hyperpolarizing Ca 2+ ‐dependent K + channels

This study deals with the modulation of the plasma membrane potential (Δψ p ) of murine erythroleukemia (MEL) cells by cell‐substratum or cell‐cell contact. Δψ p was determined by measuring the distribution of tetraphenylphosphonium (TPP + ) across the plasma membrane; it appeared strongly, and inversely, influenced by the two types of cell contacts. Contact with the culture surface produced a Δψ p hyperpolarization directly proportional to average distance among the ideal centers of the cells on this surface (d) within the range 10–80 μm. A detailed mathematical analysis of the function Δψ p = f(d) is presented, as well as experiments involving the use of ionophores (valinomycin and A23187) and the conditioning of the culture surface. We concluded that the d‐dependent hyperpolarization (dDH) was the result of a complex interplay between the activating properties of substratum on Ca 2+ ‐dependent K + channels (K Ca ) and some substratum‐adherent factors that are shed by MEL cells and antagonize K Ca activation (substratum‐attached cellular factors = SACF), By contrast, contact of the cells with each other, obtained by incubating MEL cells at d smaller than the average cell diameter (Φ = 10 μm), produced a marked Δψ p depolarization. This intercellular contact‐dependent depolarization (ICDD) was unaffected by valinomycin; it was abolished by substituting Na + in the external medium with a nondiffusible cation (choline), which shows that ICDD was sustained by Na + influxes, probably mediated by stretch‐activated (s.a.) cation channels.