@article{APS7527,
author = {Rui-Bing Su and Jin Li and Xin Li and Bo-Yi Qin},
title = {Down-regulation of MAO-B activity and imidazoline receptors in rat brain following chronic treatment of morphine},
journal = {Acta Pharmacologica Sinica},
volume = {22},
number = {7},
year = {2016},
keywords = {},
abstract = {Aim: To study the regulation of monoamine oxidase-B (MAO-B) activity and imidazoline receptors (I-R) during long term treatment of morphine.
Methods: MAO-B activity was detected by high performance liquid chromatography; I-R was detected by [3H]idazoxan binding test.
Results: Idazoxan and morphine inhibited whole brain homogenate MAO-B activity in a dose-dependent manner, while agmatine, an endogenous imidazoline ligand, didn't affect the activity of MAO-B, and it had no effect on the inhibition of MAO-B activity by idazoxan or morphine. MAO-B activity of rats decreased markedly in all five brain regions detected (cerebral cortex, hippocampus, thalamus, cerebellum, and striatum) after chronic administration of morphine for 16 d (P < 0.01). Acute challenge with naloxone or idazoxan did not influence MAO-B activity in morphine chronically treated rats. Although agmatine itself did not affect MAO-B activity, co-administration of agmatine with morphine could reverse the effect of morphine on MAO-B activity. Chronic administration of morphine significantly decreased the density of [3H]idazoxan binding sites and increased the binding affinity in cerebral cortex and cerebellum (P < 0.05 or P < 0.01).
Conclusion: MAO-B activity was relevant to the abstinent syndrome of morphine dependent rats, but not related to the effect of agmatine on morphine analgesia; influence of agmatine on the pharmacological effects of morphine was based on its activation of imidazoline receptors.},
issn = {1745-7254}, url = {http://www.chinaphar.com/article/view/7527}
}