author_facet Arabian, Maedeh
Aboutaleb, Nahid
Soleimani, Mansoureh
Ajami, Marjan
Habibey, Rouhollah
Rezaei, Yousef
Pazoki-Toroudi, Hamidreza
Arabian, Maedeh
Aboutaleb, Nahid
Soleimani, Mansoureh
Ajami, Marjan
Habibey, Rouhollah
Rezaei, Yousef
Pazoki-Toroudi, Hamidreza
author Arabian, Maedeh
Aboutaleb, Nahid
Soleimani, Mansoureh
Ajami, Marjan
Habibey, Rouhollah
Rezaei, Yousef
Pazoki-Toroudi, Hamidreza
spellingShingle Arabian, Maedeh
Aboutaleb, Nahid
Soleimani, Mansoureh
Ajami, Marjan
Habibey, Rouhollah
Rezaei, Yousef
Pazoki-Toroudi, Hamidreza
Canadian Journal of Physiology and Pharmacology
Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
Physiology (medical)
Pharmacology
General Medicine
Physiology
author_sort arabian, maedeh
spelling Arabian, Maedeh Aboutaleb, Nahid Soleimani, Mansoureh Ajami, Marjan Habibey, Rouhollah Rezaei, Yousef Pazoki-Toroudi, Hamidreza 0008-4212 1205-7541 Canadian Science Publishing Physiology (medical) Pharmacology General Medicine Physiology http://dx.doi.org/10.1139/cjpp-2017-0245 <jats:p> 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 &lt; 0.05 vs. untreated I/R) and increase in the expression of p-mTOR (P &lt; 0.05 vs. untreated I/R) and SOD activity (P &lt; 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. </jats:p> Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway Canadian Journal of Physiology and Pharmacology
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title Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_unstemmed Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_full Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_fullStr Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_full_unstemmed Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_short Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_sort preconditioning with morphine protects hippocampal ca1 neurons from ischemia–reperfusion injury via activation of the mtor pathway
topic Physiology (medical)
Pharmacology
General Medicine
Physiology
url http://dx.doi.org/10.1139/cjpp-2017-0245
publishDate 2018
physical 80-87
description <jats:p> 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 &lt; 0.05 vs. untreated I/R) and increase in the expression of p-mTOR (P &lt; 0.05 vs. untreated I/R) and SOD activity (P &lt; 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. </jats:p>
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author Arabian, Maedeh, Aboutaleb, Nahid, Soleimani, Mansoureh, Ajami, Marjan, Habibey, Rouhollah, Rezaei, Yousef, Pazoki-Toroudi, Hamidreza
author_facet Arabian, Maedeh, Aboutaleb, Nahid, Soleimani, Mansoureh, Ajami, Marjan, Habibey, Rouhollah, Rezaei, Yousef, Pazoki-Toroudi, Hamidreza, Arabian, Maedeh, Aboutaleb, Nahid, Soleimani, Mansoureh, Ajami, Marjan, Habibey, Rouhollah, Rezaei, Yousef, Pazoki-Toroudi, Hamidreza
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container_title Canadian Journal of Physiology and Pharmacology
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description <jats:p> 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 &lt; 0.05 vs. untreated I/R) and increase in the expression of p-mTOR (P &lt; 0.05 vs. untreated I/R) and SOD activity (P &lt; 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. </jats:p>
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spelling Arabian, Maedeh Aboutaleb, Nahid Soleimani, Mansoureh Ajami, Marjan Habibey, Rouhollah Rezaei, Yousef Pazoki-Toroudi, Hamidreza 0008-4212 1205-7541 Canadian Science Publishing Physiology (medical) Pharmacology General Medicine Physiology http://dx.doi.org/10.1139/cjpp-2017-0245 <jats:p> 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 &lt; 0.05 vs. untreated I/R) and increase in the expression of p-mTOR (P &lt; 0.05 vs. untreated I/R) and SOD activity (P &lt; 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. </jats:p> Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway Canadian Journal of Physiology and Pharmacology
spellingShingle Arabian, Maedeh, Aboutaleb, Nahid, Soleimani, Mansoureh, Ajami, Marjan, Habibey, Rouhollah, Rezaei, Yousef, Pazoki-Toroudi, Hamidreza, Canadian Journal of Physiology and Pharmacology, Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway, Physiology (medical), Pharmacology, General Medicine, Physiology
title Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_full Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_fullStr Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_full_unstemmed Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_short Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
title_sort preconditioning with morphine protects hippocampal ca1 neurons from ischemia–reperfusion injury via activation of the mtor pathway
title_unstemmed Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway
topic Physiology (medical), Pharmacology, General Medicine, Physiology
url http://dx.doi.org/10.1139/cjpp-2017-0245