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Mu Opioid Receptor Stimulation Activates c-Jun N-Terminal Kinase 2 by Distinct Arrestin-Dependent and Independent Mechanisms.
This study resolves distinct ligand-directed mechanisms of JNK activation by mu opioid agonists and understanding ligand-directed signaling at MOR may improve opioid therapeutics. PMID: 26056051 [PubMed - as supplied by publisher]
Source: Cellular Signalling - June 5, 2015 Category: Cytology Authors: Kuhar JR, Bedini A, Melief EJ, Chiu YC, Striegel HN, Chavkin C Tags: Cell Signal Source Type: research

Role for engagement of β‐arrestin 2 by the transactivated EGFR in agonist‐specific regulation of δ receptor activation of ERK1/2
Conclusions and Implicationsδ Receptor‐mediated activation of ERK1/2 is via ligand‐specific transactivation of EGFR. This study gains a new insight into the mechanism by which δ receptor activates ERK1/2.
Source: British Journal of Pharmacology - July 25, 2015 Category: Drugs & Pharmacology Authors: Le‐Sha Zhang, Yu‐Jun Wang, Yun‐Yue Ju, Gui‐Ying Zan, Chi Xu, Min‐Hua Hong, Yu‐Hua Wang, Zhi‐Qiang Chi, Jing‐Gen Liu Tags: RESEARCH PAPER Source Type: research

Role for engagement of β‐arrestin2 by the transactivated EGFR in agonist‐specific regulation of δ receptor activation of ERK1/2
Conclusions and ImplicationsThe δ receptor‐mediated activation of ERK1/2 is via ligand‐specific transactivation of EGFR. This study adds new insights into the mechanism by which δ receptors activate ERK1/2.
Source: British Journal of Pharmacology - September 23, 2015 Category: Drugs & Pharmacology Authors: Le‐Sha Zhang, Yu‐Jun Wang, Yun‐Yue Ju, Gui‐Ying Zan, Chi Xu, Min‐Hua Hong, Yu‐Hua Wang, Zhi‐Qiang Chi, Jing‐Gen Liu Tags: RESEARCH PAPER Source Type: research

Opioid Receptor Expression in Neuropathic Pain Neurobiology
In this study, we determined the role of G9a in diminished MOR expression and opioid analgesic effects in animal models of neuropathic pain. We found that nerve injury in rats induced a long-lasting reduction in the expression level of MORs in the DRG but not in the spinal cord. Nerve injury consistently increased the enrichment of the G9a product histone 3 at lysine 9 dimethylation in the promoter of Oprm1 in the DRG. G9a inhibition or siRNA knockdown fully reversed MOR expression in the injured DRG and potentiated the morphine effect on pain hypersensitivity induced by nerve injury. In mice lacking Ehmt2 in DRG neurons, ...
Source: Journal of Biological Chemistry - April 14, 2016 Category: Chemistry Authors: Zhang, Y., Chen, S.-R., Laumet, G., Chen, H., Pan, H.-L. Tags: Molecular Bases of Disease Source Type: research

Activation of NPFFR2 leads to hyperalgesia through the spinal inflammatory mediator CGRP in mice.
Abstract Neuropeptide FF (NPFF) is recognized as an opioid modulating peptide that regulates morphine-induced analgesia. The aim of this study was to delineate the role of NPFFR2 in pain transmission. We found the expression levels of NPFF and NPFFR2 were increased in the lumbar dorsal horn of animals with CFA- and carrageenan-induced inflammation and both NPFFR2 over-expressing transgenic (NPFFR2-Tg) and NPFFR2 agonist-treated mice displayed hyperalgesia. BOLD signals from functional MRI showed that NPFFR2-Tg mice exhibited increased activation of pain-related brain regions after painful stimulation when compared...
Source: Experimental Neurology - February 4, 2017 Category: Neurology Authors: Lin YT, Liu HL, Day YJ, Chang CC, Hsu PH, Chen JC Tags: Exp Neurol Source Type: research

Contribution of dorsal root ganglion octamer transcription factor 1 to neuropathic pain after peripheral nerve injury
In this study, we investigated whether octamer transcription factor 1 (OCT1), a transcription factor, contributed to neuropathic pain caused by chronic constriction injury (CCI) of the sciatic nerve. Chronic constriction injury produced a time-dependent increase in the level of OCT1 protein in the ipsilateral L4/5 DRG, but not in the spinal cord. Blocking this increase through microinjection of OCT1 siRNA into the ipsilateral L4/5 DRG attenuated the initiation and maintenance of CCI-induced mechanical allodynia, heat hyperalgesia, and cold allodynia and improved morphine analgesia after CCI, without affecting basal respons...
Source: Pain - January 24, 2019 Category: Anesthesiology Tags: Research Paper Source Type: research

Why Do Birds Flock? A Role for Opioids in the Reinforcement of Gregarious Social Interactions
Conclusion We propose that studies of songbirds reveal a novel network model for the integration of positive and negative reinforcement processes in non-sexual affiliative social behavior. Most studies on affiliative behavior focus on the positive affective state induced by social contact that rewards individuals interacting together. However, this review highlights that in social animals, affiliative contact is also reinforced because it reduces a negative affective state caused by social exclusion or isolation, thus creating a complementary system (i.e., positive reinforcement from affiliative interactions and negative ...
Source: Frontiers in Physiology - April 11, 2019 Category: Physiology Source Type: research

Connecting Metainflammation and Neuroinflammation Through the PTN-MK-RPTP β/ζ Axis: Relevance in Therapeutic Development
Conclusion The expression of the components of the PTN-MK-RPTPβ/ζ axis in immune cells and in inflammatory diseases suggests important roles for this axis in inflammation. Pleiotrophin has been recently identified as a limiting factor of metainflammation, a chronic pathological state that contributes to neuroinflammation and neurodegeneration. Pleiotrophin also seems to potentiate acute neuroinflammation independently of the inflammatory stimulus while MK seems to play different -even opposite- roles in acute neuroinflammation depending on the stimulus. Which are the functions of MK and PTN in chronic neuroi...
Source: Frontiers in Pharmacology - April 11, 2019 Category: Drugs & Pharmacology Source Type: research

Long non-coding RNA MEG3 attends to morphine-mediated autophagy of HT22 cells through modulating ERK pathway.
Conclusions: Up-regulation of MEG3 attended to the morphine-caused autophagy of HT22 cells might be through elevating c-fos expression and promoting ERK pathway activation. More experiments are also needed in the future to analyse the influence of other lncRNAs in drug addiction. PMID: 31433241 [PubMed - in process]
Source: Pharmaceutical Biology - August 22, 2019 Category: Drugs & Pharmacology Tags: Pharm Biol Source Type: research

Morphine Prevents Ischemia/Reperfusion-Induced Myocardial Mitochondrial Damage by Activating δ-opioid Receptor/EGFR/ROS Pathway
ConclusionsMorphine may prevent I/R-induced myocardial mitochondrial damage by activating EGFR through δ-opioid receptors, in turn increasing RISK and SAFE pathway activity via intracellular ROS. Moreover, morphine may reduce myocardial injury by regulating autophagy but not apoptosis.
Source: Cardiovascular Drugs and Therapy - September 28, 2022 Category: Cardiology Source Type: research

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