Regulation by calcium of short-term plasticity of the cholinoreceptors of RPa3 and LPa3 neurons of the edible snail.

The pharmacological influences which change the intracellular content of free Ca2+ reversibly change the rate and depth of the extinction of the inward current of RPa3 and LPa3 neurons of the edible snail, elicited by repeated iontophoretic applications of acetylcholine to the soma. Suppression by a calcium-free extracellular medium and by verapamil (100-150 mumoles/liter) of the influx of Ca2+ into the cell, induced by the activation of cholinoreceptors, reversibly attenuates the extinction. An increase in the level of intracellular Ca2+ by ruthenium red blockade (5-10 mumoles/liter) of the specific transport of Ca2+ by the mitochondria and by caffeine mobilization (1-4 mmoles/liter) of Ca2+ deposited by the endoplasmic reticulum increases and intensifies extinction. The results obtained indicate that the short-term plasticity of the cholinoreceptors of these neurons is positively regulated by Ca2+ which has entered the cell along chemoregulated ion channels, and has been mobilized from the intracellular Ca depots.