45Ca displacement related to pharmacologically induced prolonged action potentials in Nitella flexilis.
Nitella cells were loaded with 45Ca2+ to an activity of 2 X 10(5) cpm. Insertion of two glass-capillary electrodes into each of six cells released varying amounts of Ca2+ in the order of 1 mumol per cell, but hyperpolarizing and depolarizing pulses up to 500 ms in duration caused no measurable loss (less than 57 pmol) of Ca2+ even when the latter elicited action potentials. Addition of 10 mumol of Ba2+ or tetraethylammonium (TEA) caused losses up to 1200 pmol of Ca2+ from the cells and prolonged the action potentials by a factor of three or more. Subsequent addition of Ba2+ or TEA to treated cells caused no further losses of Ca. Because prolonged action potentials can apparently only be elicited after the chelation or displacement of Ca2+, we propose that, as in many animal cells, the K+ channels responsible for the normal brief repolarizing phase of the action potential are controlled by Ca2+ in these electrically excitable plant cells.
D000200:Action Potentials / Q000187:drug effects; D001464:Barium / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D000460:Chlorophyta / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D004558:Electric Stimulation; D008564:Membrane Potentials / Q000187:drug effects; D013757:Tetraethylammonium Compounds / Q000494:pharmacology
D013757:Tetraethylammonium Compounds; D001464:Barium; D002118:Calcium