Related Experiment Video
Updated: Jul 20, 2026

Operant Protocols for Assessing the Cost-benefit Analysis During Reinforced Decision Making by Rodents
Published on: September 10, 2018
Modulation of agmatine on calcium signal in morphine-dependent CHO cells by activation of IRAS, a candidate for
1Beijing Institute of Pharmacology and Toxicology, 27th Taiping Road, Beijing 100850, China.
Abstract:
The present study investigated the effects of agmatine action on imidazoline I1 receptor antisera-selected protein (IRAS), a candidate for imidazoline I1 receptor, on prolonged morphine-induced adaptations of calcium signal and long-lasting alterations in gene expression to further elucidate the role of IRAS in opioid dependence. Two cell lines, Chinese hamster ovary cells expressing mu opioid receptor alone (CHO-mu) and expressing mu opioid receptor and IRAS together (CHO-mu/IRAS), were used. After chronic treatment with morphine for 48 h, naloxone induced a significant elevation of intracellular calcium concentration ([Ca2+]i) in CHO-mu and CHO-mu/IRAS cells. Agmatine (0.01-3 microM) concentration-dependently inhibited the naloxone-precipitated [Ca2+]i elevation when co-pretreated with morphine in CHO-mu/IRAS, but not in CHO-mu. Efaroxan, an imidazoline I1 receptor-preferential antagonist, completely reversed the effect of agmatine in CHO-mu/IRAS. Agmatine (1-10 microM) administration after chronic morphine exposure for 48 h partially decreased the [Ca2+]i elevation in CHO-mu/IRAS which was entirely antagonized by efaroxan, but not in CHO-mu. In addition, agmatine (1 microM) co-pretreated with morphine attenuated the naloxone-precipitated increases of cAMP-responsive element binding protein and extracellular signal-regulated kinase 1/2 phosphorylations and c-Fos expression in CHO-mu/IRAS. These effects were blocked by efaroxan as well. Taken together, these results indicate that the agmatine-IRAS action system attenuates the up-regulations of Ca2+ signal and its downstream gene expression in morphine-dependent model in vitro, providing additional evidence to support the contribution of IRAS to opioid dependence.
More Related Videos
07:41A Kinetic Fluorescence-based Ca2+ Mobilization Assay to Identify G Protein-coupled Receptor Agonists, Antagonists, and Allosteric Modulators
Published on: February 20, 2018
09:09Preparation and Delivery of Protein Microcrystals in Lipidic Cubic Phase for Serial Femtosecond Crystallography
Published on: September 20, 2016
Related Concept Videos
Opioid Receptors: Overview
Calmodulin-dependent Signaling
The Ca2+-CaM complex does not have enzymatic activity by itself. Instead, the complex binds downstream target proteins, including membrane proteins or enzymes,...
IP3/DAG Signaling Pathway
Analgesia and Pain Management
G-Protein Gated Ion Channels
Sensory organs,...
Ligand-Gated Ion Channel Receptor: Gating Mechanism