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Depressing Effects of Protein Kinases a & c on the Receptor-Induced K+-Current Responses in the Ganglion Cells of Aplysia

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For more content, see Archives Néerlandaises de Zoologie (Vol 1-17) and Animal Biology (Vol 53 and onwards).

Application of either dopamine (DA), acetylcholine (ACh), histamine (HA), or Phe-Met-Arg-Phe-NH2 (FMRFamide) induces a K+-current response in the ganglion cells of Aplysia under voltage clamp. We have previously reported that these responses are all mediated by a pertussis toxin (PTX)-sensitive G-protcin Gi or Go. Intracellular application of cAMP, an activator of protein kinase A (PKA), or extracellular application of 30 μM phorbol dibutyrate (PDBu), an activator of protein kinase C (PKC), markedly suppressed these transmitter-induced K+-current responses. The depressing effect of cAMP was reversible while that of PDBu was irreversible as observed for 1 hour. Intracellular injection of the catalytic subunit of either PKA or PKC mimicked the effects of cAMP or PDBu. Pretreatment of the ganglion cells with 100 μM H-7, an inhibitor of PKC, significantly suppressed the effect of PDBu. Furthermore, an intraccllular injection of okadaic acid (OA), an inhibitor of phosphatases, facilitated the blocking effects of both cAMP and PDBu. The dose-response curve obtained by each transmitter-receptor system shifted downward by application of either cAMP or PDBu without affecting the affinity of the agonist to each receptor. K+-channel opening directly induced by guanosine thiotriphosphate (GTPγS) or by raising the temperature was not depressed by cither cAMP or 100 μM PDBu. From these results, we postulated that the acting sites of both PKA and PKC might be somewhere between the receptors and G-protein, and that the phosphorylation of these sites would impair the functional coupling efficiency between the receptors and G-protein.

Affiliations: 1: Department of Physiology, School of Medicine, Iwate Medical University, Morioka 020, Japan

10.1163/156854293X00638
/content/journals/10.1163/156854293x00638
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/content/journals/10.1163/156854293x00638
1993-01-01
2016-12-07

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