Evidence that Ca2+/calmodulin-dependent protein phosphorylation is involved in the opening process of potassium channels in identified snail neurons

• Published in: Neuroscience letters Vol. 124; no. 1; p. 35
• Main Authors: Onozuka, M, Furuichi, H, Imai, S, Fukami, Y
• Format: Journal Article
• Language: English
• Published: Ireland 11.03.1991
• Subjects: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; Animals; Calcium - physiology; Calcium-Calmodulin-Dependent Protein Kinases; Calmodulin - antagonists & inhibitors; Calmodulin - physiology; Ion Channel Gating - drug effects; Ion Channel Gating - physiology; Isoquinolines - pharmacology; Neurons - drug effects; Neurons - physiology; Phosphorylation - drug effects; Piperazines - pharmacology; Potassium Channels - drug effects; Potassium Channels - physiology; Protein Kinase Inhibitors; Protein Kinases - physiology; Protein Processing, Post-Translational - drug effects; Snails; Sulfonamides - pharmacology; Tetraethylammonium; Tetraethylammonium Compounds - pharmacology
• ISSN: 0304-3940
• DOI: 10.1016/0304-3940(91)90816-C

The effect of Ca2+/calmodulin-dependent protein phosphorylation on K+ channels was examined in snail neurons, using several pharmacological agents, the voltage clamp method and the pressure injection technique. H-7, a general protein kinase inhibitor, reduced the delayed outward K+ current (IKD) which was suppressed by tetraethylammonium. Ca2+/calmodulin-dependent protein kinase II, when injected into neurons which had been treated with H-7, transiently restored the reduced IKD nearly to the pre-H-7 level. However, this restoration was blocked by W-7, a calmodulin inhibitor. In contrast, the catalytic subunit of cAMP-dependent protein kinase or protein kinase C injected into the H-7-treated neurons had little effect on the current. These findings suggest that Ca2+/calmodulin-dependent protein phosphorylation is involved in the opening process of K+ channels.