Preconditioning with morphine protects hippocampal CA1 neurons from ischemia�reperfusion injury via activation of the mTOR pathway

Arabian, M. and Aboutaleb, N. and Soleimani, M. and Ajami, M. and Habibey, R. and Rezaei, Y. and Pazoki-Toroudi, H. (2018) Preconditioning with morphine protects hippocampal CA1 neurons from ischemia�reperfusion injury via activation of the mTOR pathway. Canadian Journal of Physiology and Pharmacology, 96 (1). pp. 80-87.

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The signaling pathway of chronic morphine treatment to prevent neuronal damage following transient cerebral ischemia is not clear. In this study, we examined the role of mammalian target of rapamycin (mTOR) to identify the neuroprotective effects of chronic morphine preconditioning on the hippocampus following ischemia�reperfusion (I/R) injury. Morphine was administered for 5 days, twice a day, before inducing I/R injury. The possible role of mTOR was evaluated by the injection of rapamycin (5 mg/kg body weight, by intraperitoneal injection) before I/R was induced. The passive avoidance test was used to evaluate memory performance. Neuronal density and apoptosis were measured in the CA1 region, 72 h after I/R injury. The expressions of mTOR and phosphorylated mTOR (p-mTOR), as well as superoxide dismutase (SOD) activity were determined 24 h after I/R injury. Chronic morphine treatment attenuated apoptosis and neuronal loss in the hippocampus after I/R injury, which led to improvement in memory (P < 0.05 vs. untreated I/R) and increase in the expression of p-mTOR (P < 0.05 vs. untreated I/R) and SOD activity (P < 0.05 vs. untreated I/R) in the hippocampus. Pretreatment with rapamycin abolished all the above-mentioned protective effects. These results describe novel findings whereby chronic morphine preconditioning in hippocampal CA1 neurons is mediated by the mTOR pathway, and through increased phosphorylation of mTOR can alleviate oxidative stress and apoptosis, and eventually protect the hippocampus from I/R injury. © 2017, Published by NRC Research Press.

Item Type: Article
Additional Information: cited By 2
Uncontrolled Keywords: morphine; neuroprotective agent; superoxide dismutase; target of rapamycin kinase, animal; apoptosis; avoidance behavior; Bagg albino mouse; drug effect; hippocampal CA1 region; male; memory; metabolism; nerve cell; pathology; phosphorylation; reaction time; reperfusion injury; signal transduction, Animals; Apoptosis; Avoidance Learning; CA1 Region, Hippocampal; Male; Memory; Mice, Inbred BALB C; Morphine; Neurons; Neuroprotective Agents; Phosphorylation; Reaction Time; Reperfusion Injury; Signal Transduction; Superoxide Dismutase; TOR Serine-Threonine Kinases
Subjects: WJ Urogenital System
Depositing User: eprints admin
Date Deposited: 29 Dec 2018 10:51
Last Modified: 29 Dec 2018 10:51

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