Effects of Ca2+ and vitamin E on posttranslational regulation of acetylcholine receptor expression in the somata of identified molluscan neurons

The effects of Ca²⁺ and vitamin E (-tocopherol) on acetylcholine (Ach)-induced Cl^– currents in LP11 and RBc4 neurons of the snail Helix pomatia have been studied. Injection of Ca²⁺ into the cells and application of vitamin E (10^–5 mole/liter) induced the appearance of potentiation of Ach-induced currents in membrane parts more remote from the axon than the Ach-sensitive regions in the control. The Hill coefficient (n) for such Ach receptors was equal to 0.8, unlike 1.8 for Ach receptors active in the control. Arachidonic acid (10^–5 mole/liter) and phorbol ester TPA (10^–6 mole/liter) inhibited Ach responses, while oleoylacetyglycerol (10^–6 mole/liter) produced no effect. Calmidazolium (10^–6 mole/liter) decreased the effects of Ca²⁺ and vitamin E on Ach responses, while nordihydroquiaretic acid (5 · 10^–6 mole/liter) enhanced the modulating effect of vitamin E and weakened that of arachidonic acid. It is suggested that the expression of Ach receptors activated by Ca²⁺ and vitamin E is mediated through posttranslational mechanisms, since cycloheximide and actinomycin D, inhibitors of protein synthesis, did not influence the effects of C²⁺ and vitamin E. The mechanisms responsible for the stimulating effects of Ca²⁺ and vitamin E are discussed.Translated from Neirofiziologiya, Vol. 25, No. 1, pp. 31–39, January–February, 1993.