The Ca2+ current evoked by hyperpolarization persisted in the presence of 100 µM Cd2+ (Fig. 5B).
Possible explanations for reduced SDtc in motor axons could be structural changes, membrane hyperpolarization, or persistently decreased Na+ conductance [11, 17, 18].
Membrane hyperpolarization was not evident.
Lubiprostone caused SC-51322-insensitive membrane hyperpolarization and no effect on [cAMP]i.
In further experiments, C8-HSL promoted membrane hyperpolarization in epidermal root cells.
Furthermore, the AHL-mediated membrane hyperpolarization is leading to increased K+ uptake of the root tissue.
Opening K+ channels triggers K+ efflux, which leading to membrane hyperpolarization, preventing Ca2+entry through closing voltage-operated Ca2+ channels.
Iontophoretic injections of chloride ions into the motoneurons reversed the polarity of the membrane hyperpolarization during the PPN stimulation.
Fluorescence microscopy observations showed that attachment of CMV particles to membrane-engineered cells was associated with membrane hyperpolarization and increased [Ca2+]cyt.
