INT26472
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Thus, the results of the present study revealed that the effects of these naltrexone pretreatments on ethanol-induced locomotion are similar to the previously described changes on MOR activity. | |||||||||||||||
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Detection of genetic variation affecting OPRM1 expression or mu opioid receptor function would be an important step towards understanding the origins of inter-individual variation in response to mu opioid receptor ligands and in diseases of substance dependence. | |||||||||||||||
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In particular, screening of genetically modified mice lacking individual GRKs or beta arrestins for alterations in behavioral and biochemical responses to cocaine and morphine has revealed a functional specificity in dopamine and mu-opioid receptor regulation of locomotion and analgesia. | |||||||||||||||
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Previous pharmacological data using antagonists with preferential actions at mu-, delta-, and kappa-opioid receptors indicate the importance of the mu-opioid receptor in mediating this effect. | |||||||||||||||
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Previous studies indicate that down-regulation of muOR is more likely with high-efficacy opioid agonists (e.g., etorphine), whereas lower efficacy agonists (e.g., morphine) do not regulate muOR density. | |||||||||||||||
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Although in vivo heterologous regulation of mu-opioid receptor mRNA by non-opioid compounds has been reported, the failure to observe changes in mu-opioid receptor mRNA levels in vivo after treatment with opioid agonists raised the possibility that in vivo homologous regulation by agonists may not occur. | |||||||||||||||
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Regulation of the mu-opioid receptor gene by opioid analgesic drugs has not been observed in rats and mice following in vivo treatments that produce tolerance. | |||||||||||||||
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Although in vivo heterologous regulation of mu-opioid receptor mRNA by non-opioid compounds has been reported, the failure to observe changes in mu-opioid receptor mRNA levels in vivo after treatment with opioid agonists raised the possibility that in vivo homologous regulation by agonists may not occur. | |||||||||||||||
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In a previous study we showed that morphine did not desensitize the cloned mu receptor even though it is a potent and effective agonist at the mu receptor. | |||||||||||||||
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These results demonstrate a significant difference between mu opioid receptor regulation in B6 and D2 mice, and may underlie well documented strain differences in specific opioid-related behaviors. | |||||||||||||||
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MOR mRNA levels in the DRG were not affected 7 days after inflammation, whereas chronic morphine administration induced a discrete increase (p < 0.05). | |||||||||||||||
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However, G((i)alpha2) is not required for agonist-induced mu-opioid receptor density regulation in vivo. | |||||||||||||||
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Modulation of hypothalamic mu-opioid receptor density by estrogen: a quantitative autoradiographic study of the female C57BL/6J mouse. | |||||||||||||||
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We demonstrate for the first time a role of PARP-1 as a transcriptional repressor in MOR gene regulation. | |||||||||||||||
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Furthermore, the differential regulation of mu-opioid receptor abundance by agonists and antagonists in immunoblotting assays contrasts with changes in [3H] DAMGO binding. | |||||||||||||||
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Delivery of the same daily dose of etorphine or naloxone using intermittent (every 24 h for 7 days) s.c. administration had no effect on immunoreactive mu-opioid receptor, [3H] DAMGO binding or dynamin-2 abundance. | |||||||||||||||
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These findings provide in vivo evidence that the muOR is differentially regulated in diverse regions of the CNS. | |||||||||||||||
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We used real-time PCR and [35S]GTPgammaS binding assays to examine the changes of MOR mRNA levels and the capability of the mu-opioid agonist peptide ([D-Ala2,(NMe)Phe4,Gly5-ol]enkephalin (DAMGO) in activating regulatory G-proteins via MORs in forebrain membrane fractions of wild-type (w.t., CB1+/+) and CB1 receptor deficient transgenic mice (knockout, CB1-/-). | |||||||||||||||
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These data show that regulation of the MOR uORF is independent of the peptide sequence of the uORF. | |||||||||||||||
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We demonstrate novel roles as transcriptional regulators in Oprm1 regulation for hnRNP K and ? | |||||||||||||||
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