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Phospholipase C-dependent hydrolysis of phosphatidylinositol 4,5-bisphosphate underlies agmatine-induced suppression of N-type Ca2+ channel in rat celiac ganglion neurons

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Title: Phospholipase C-dependent hydrolysis of phosphatidylinositol 4,5-bisphosphate underlies agmatine-induced suppression of N-type Ca2+ channel in rat celiac ganglion neurons
Authors: Young-Hwan Kim, Ji-Hyun Jeong, Duck-Sun Ahn, Seungsoo Chung
Contributors: College of Medicine, Dept. of Physiology, Young-Hwan Kim, Ji-Hyun Jeong, Duck-Sun Ahn, Seungsoo Chung, Kim, Young Hwan, Ahn, Duk Sun, Chung, Seung Soo
Source: Biochemical and Biophysical Research Communications. 484:342-347
Publisher Information: Elsevier BV, 2017.
Publication Year: 2017
Subject Terms: Calcium Channel Blockers/pharmacology, Male, Phosphatidylinositol 4,5-Diphosphate, 0301 basic medicine, Agmatine, Neurons/metabolism, Imidazoline receptor, Phosphatidylinositol 4,5-Diphosphate/metabolism, Rats, Sprague-Dawley, 03 medical and health sciences, Calcium Channels, N-Type, Abdomen, Type C Phospholipases/metabolism, Animals, Neurons, 0303 health sciences, Ganglia, Sympathetic, Hydrolysis, Calcium Channel Blockers, Neurons/drug effects, Sympathetic/metabolism, Rats, 3. Good health, N-Type/drug effects, Type C Phospholipases, Ganglia, Phosphatidylinositol 4,5-bisphosphate, Calcium Channels, Sympathetic/drug effects, Sprague-Dawley, Agmatine/pharmacology, Cav2.2
Description: Agmatine suppresses peripheral sympathetic tone by modulating Cav2.2 channels in peripheral sympathetic neurons. However, the detailed cellular signaling mechanism underlying the agmatine-induced Cav2.2 inhibition remains unclear. Therefore, in the present study, we investigated the electrophysiological mechanism for the agmatine-induced inhibition of Cav2.2 current (ICav2.2) in rat celiac ganglion (CG) neurons. Consistent with previous reports, agmatine inhibited ICav2.2 in a VI manner. The agmatine-induced inhibition of the ICav2.2 current was also almost completely hindered by the blockade of the imidazoline I2 receptor (IR2), and an IR2 agonist mimicked the inhibitory effect of agmatine on ICav2.2, implying involvement of IR2. The agmatine-induced ICav2.2 inhibition was significantly hampered by the blockade of G protein or phospholipase C (PLC), but not by the pretreatment with pertussis toxin. In addition, diC8-phosphatidylinositol 4,5-bisphosphate (PIP2) dialysis nearly completely hampered agmatine-induced inhibition, which became irreversible when PIP2 resynthesis was blocked. These results suggest that in rat peripheral sympathetic neurons, agmatine-induced IR2 activation suppresses Cav2.2 channel voltage-independently, and that the PLC-dependent PIP2 hydrolysis is responsible for the agmatine-induced suppression of the Cav2.2 channel.
Document Type: Article
Language: English
ISSN: 0006-291X
DOI: 10.1016/j.bbrc.2017.01.120
Access URL: https://pubmed.ncbi.nlm.nih.gov/28131838
https://www.sciencedirect.com/science/article/pii/S0006291X17301791
https://www.sciencedirect.com/science/article/pii/S0006291X17301791#!
http://europepmc.org/abstract/MED/28131838
http://www.sciencedirect.com/science/article/pii/S0006291X17301791
https://pubmed.ncbi.nlm.nih.gov/28131838/
https://www.ncbi.nlm.nih.gov/pubmed/28131838
Rights: Elsevier TDM
CC BY NC ND
Accession Number: edsair.doi.dedup.....e7cd1f62e5e87c0b6e3719338dd17e97
Database: OpenAIRE
Description
Abstract:Agmatine suppresses peripheral sympathetic tone by modulating Cav2.2 channels in peripheral sympathetic neurons. However, the detailed cellular signaling mechanism underlying the agmatine-induced Cav2.2 inhibition remains unclear. Therefore, in the present study, we investigated the electrophysiological mechanism for the agmatine-induced inhibition of Cav2.2 current (ICav2.2) in rat celiac ganglion (CG) neurons. Consistent with previous reports, agmatine inhibited ICav2.2 in a VI manner. The agmatine-induced inhibition of the ICav2.2 current was also almost completely hindered by the blockade of the imidazoline I2 receptor (IR2), and an IR2 agonist mimicked the inhibitory effect of agmatine on ICav2.2, implying involvement of IR2. The agmatine-induced ICav2.2 inhibition was significantly hampered by the blockade of G protein or phospholipase C (PLC), but not by the pretreatment with pertussis toxin. In addition, diC8-phosphatidylinositol 4,5-bisphosphate (PIP2) dialysis nearly completely hampered agmatine-induced inhibition, which became irreversible when PIP2 resynthesis was blocked. These results suggest that in rat peripheral sympathetic neurons, agmatine-induced IR2 activation suppresses Cav2.2 channel voltage-independently, and that the PLC-dependent PIP2 hydrolysis is responsible for the agmatine-induced suppression of the Cav2.2 channel.
ISSN:0006291X
DOI:10.1016/j.bbrc.2017.01.120