EPYLRFamide-mediated reduction of acetylcholine-induced inward currents in Helix lucorum-identified neurones: role of NAADP-dependent and IP3-dependent Ca2+ release from internal stores, calmodulin and Ca2+/calmodulin-dependent protein kinase II

Pivovarov, Arkady S and Walker, Robert J. (2003) EPYLRFamide-mediated reduction of acetylcholine-induced inward currents in Helix lucorum-identified neurones: role of NAADP-dependent and IP3-dependent Ca2+ release from internal stores, calmodulin and Ca2+/calmodulin-dependent protein kinase II. Regulatory Peptides, 111 (1-3), 31-39. (doi:10.1016/S0167-0115(02)00221-5).

Abstract

The effect of seven compounds intracellularly applied by spontaneous diffusion were investigated on the EPYLRFamide-induced reduction of acetylcholine-induced inward current (ACh-current) recorded from identified neurones from Helix lucorum. Inward currents were recorded from neurones LPa2, LPa3, RPa3 and RPa2 in isolated ganglia preparations using two-electrode voltage clamp technique. ACh was applied ionophoretically.

Heparin, an antagonist of IP3 receptors (IP3Rs), and IP3, the agonist of IP3Rs, decreased the effect of EPYLRFamide. Thio-NADP, a blocker of NAADP-induced Ca2+ release, ?-NAADP, Ca2+ releaser, R24571, W-7 (both calmodulin antagonists), and KN-62, a selective inhibitor of Ca2+/calmodulin-dependent protein kinase II, did not change the modulatory effect of EPYLRFamide. These data suggest that EPYLRFamide decreases ACh-current through elevation of the basal intracellular level of the putative endogenous agonist of IP3Rs which activates release of Ca2+ from intracellular stores. It is concluded that intracellular free Ca2+ acts on ACh receptor/ionic channel without activation of calmodulin and Ca2+/calmodulin-dependent protein kinase II

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Contributors

Author: Robert J. Walker

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