Arachidonic acid and its acyclic derivatives regulate short-term plasticity of the cholinoreceptors of neurons of the edible snail.

The influence of eicosanoids on the dynamics of the extinction of the inward current, induced by repeated iontophoretic applications of acetylcholine to the soma has been demonstrated in identified RPa3 and LPa3 neurons of the edible snail by means of bielectrode recording of the membrane potential. The extracellular action of arachidonic acid (50-100 mumole/l) intensifies the extinction. Quinacrine (100-600 mumole/l), an inhibitor of phospholipase A2, which decreases the content of arachidonic acid in the cells, acts ambiguously. Nordihydroguaiaretic acid (3-10 mumole/l), which is an inhibitor of the lipoxygenase oxidation of arachidonic acid, attenuates the extinction. Indomethacin (10-50 mumole/l), a blocker of cyclooxygenase oxidation of arachidonic acid, does not influence extinction. All of the compounds investigated decrease the amplitude of the inward current induced by acetylcholine. The results obtained make it possible to hypothesize that arachidonic acid and its acyclic metabolites, which are formed as a result of lipoxygenase oxidation, regulate short-term plasticity of the cholinoreceptors of neurons of the edible snail. The cyclic eicosanoids which are formed during the cyclooxygenase oxidation of arachidonic acid do not exert a regulatory effect on the plasticity of the cholinoreceptors.