Regulatory roles of Ca2+/calmodulin-dependent protein kinase II and protein phosphatase 2A on the quisqualic acid-induced K+-current response in identified neurons of Aplysia

• Published in: Neuroscience research Vol. 60; no. 1; pp. 73 - 81
• Main Authors: Kimura, Shingo, Kawasaki, Satoshi, Watanabe, Shuji, Fujita, Reiko, Sasaki, Kazuhiko
• Format: Journal Article
• Language: English
• Published: Ireland 01.01.2008
• Subjects: Action Potentials - drug effects; Action Potentials - physiology; Animals; Aplysia - cytology; Aplysia - metabolism; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - antagonists & inhibitors; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - physiology; Cell Membrane - drug effects; Cell Membrane - metabolism; Enzyme Inhibitors - pharmacology; Excitatory Amino Acid Agonists - pharmacology; Ganglia, Invertebrate - cytology; Ganglia, Invertebrate - drug effects; Ganglia, Invertebrate - metabolism; Ion Channel Gating - drug effects; Ion Channel Gating - physiology; Membrane Potentials - drug effects; Membrane Potentials - physiology; Nervous System - cytology; Nervous System - drug effects; Nervous System - metabolism; Neural Inhibition - drug effects; Neural Inhibition - physiology; Neurons - cytology; Neurons - drug effects; Neurons - metabolism; Patch-Clamp Techniques; Potassium Channels - drug effects; Potassium Channels - metabolism; Protein Phosphatase 2 - antagonists & inhibitors; Protein Phosphatase 2 - physiology; Quisqualic Acid - pharmacology; Synaptic Transmission - drug effects; Synaptic Transmission - physiology
• ISSN: 0168-0102
• DOI: 10.1016/j.neures.2007.09.007

In identified B6 neurons of Aplysia buccal ganglia under voltage-clamp, application of quisqualic acid (QA) induces a unique slow K(+)-current response independent of G-protein. The response was augmented by raising the temperature in a similar fashion to the Phe-Met-Arg-Phe-NH(2)-induced K(+)-current response mediated by Gi/o. The QA-induced K(+)-current response markedly increased during the perfusion with Ca(2+)-free solution or after the application of W-7, a calmodulin (CaM) inhibitor. It was also enhanced by intracellular application either of H-7, a serine/threonine protein kinase inhibitor, or of KN-93, a Ca(2+)/CaM-dependent kinase II (CaMKII) inhibitor. Furthermore, the QA-induced response was markedly augmented by pre-treatment with 2,3-butanedione monoxime, an inorganic phosphatase. Intracellular application of protein phosphatase 2A (PP2A) significantly augmented the QA-induced response although neither protein phosphatase 1 nor protein phosphatase 2B altered the response. Application of either okadaic acid or calyculin A, protein phosphatase inhibitors, only slightly depressed the QA-induced response. Surprisingly, W-7 had no augmenting effect on the QA-induced response when examined after the application of either okadaic acid or calyculin A. These results suggest that the K(+)-current response is reciprocally but sequentially regulated by PP2A and CaMKII, the response of which the former is facilitating and the latter is inhibiting.