Involvement of Na/Ca exchange and intracellular mobilized Ca2+ in Na,K-pump-mediated control of depression of the cholinosensitivy of common snail neurons [correction of neorons] using a cellular analog of habituation.

The role of Na/Ca exchange and intracellular mobilized Ca2+ in modifying the depression of defensive behavior command neuron cholinosensitivity induced by the the Na,K pump inhibitor ouabain was studied in common snails using a cellular analog of habituation. Integral transmembrane acetylcholine-evoked currents (ACh currents) were recorded using a two-electrode membrane potential clamping technique. Decreases in neuron cholinosensitivity in the cellular analog of habituation were assessed in terms of the depth of depression of the amplitude of ACh currents during rhythmic local application of acetylcholine (with interstimulus intervals of 2-4 min) to the somatic membrane. The Na/Ca exchange inhibitor benzamyl (applied extracellularly, 15-35 microM) and two specific endoplasmic reticulum Ca-ATPase inhibitors, cyclopiazonic acid and thapsigargin (applied intracellularly. 0.1 mM) prevented modification of depression of the ACh current by ouabain (100 microM). It is concluded that Na/Ca exchange and the release of mobilized Ca2+ from intracellular calcium depots are involved in the mechanism by which the Na,K pump controls the depression of neuron cholinosensitivity in the cellular analog of habituation.