Calcium influx in molluscan neurons enhances the acetylcholine-induced current: The role of calmodulin

Abstract

1. Intracellular recordings were made from identified LPL1, RBc4, D1 and E4 neurons in perioesophageal ganglionic ring with buccal ganglia of the mollusc Helix pomatia. 2. The modulations of acetylcholine (ACh) receptor activity by calcium influx and cyclic adenosine monophosphate (cyclic AMP) in these neurons were investigated using two-microelectrode intracellular recording and voltage clamp techniques. 3. The elevation of calcium and cyclic AMP levels to the same identified LP11 and RBc4 neurons was shown to produce antagonistic effects on the ACh-induced chloride current. 4. The calcium influx in LP11 and RBc4 neurons triggered secondary mechanisms, which led to enhancement of the ACh-induced chloride current in these neurons. 5. Calcium influx and elevation of intracellular cyclic AMP levels both induced a decrease of ACh-induced chloride current in the same identified D1 and E4 neurons. 6. The calmodulin inhibitor chloropromazine (6.10 −5M) inhibited the enhancing effect of calcium influx on ACh-induced currents in LP11 and RBc4 neurons, but it was ineffective for D1 and E4 neurons. 7. Moreover, the inhibitor of calcium-phospholipid-dependent protein kinase polymixin B (10 −4M) had no effect on the modulations of ACh receptor activity by calcium influx in LP11, RBc4, D1 and E4 neurons. 8. These results suggest that calcium influx may activate calcium/calmodulin-dependent phosphorylation of ACh receptors on LP11 and RBc4 neurons, which evoke the essential enhancement of ACh-induced chloride current.