INT20845
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Additionally, it is suggested that chronic exposure to pain produces a constant elevation of opioid peptides leading to opioid receptor downregulation and consequently morphine tolerance. | |||||||||||||||
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Previous study has demonstrated that chronic treatment of [D-Ala2,D-Leu5] enkephalin (DADLE) induces profound down-regulation of delta opioid receptor in rat brain. | |||||||||||||||
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Delta opioid receptor down-regulation is independent of functional G protein yet is dependent on agonist efficacy. | |||||||||||||||
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Chronic opioid treatment of neuroblastoma x glioma NG108-15 cells induces desensitization of the opioid receptor and this may involve a change in membrane protein phosphorylation. | |||||||||||||||
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In summary, except the opioid receptor uncoupling and opioid receptor down-regulation, chronic morphine treatment may also activate pain facilitatory systems (NMDA receptor activation, NO production, and COX ac-tivation) during opioid tolerance development. | |||||||||||||||
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FHP subjects had greater ACTH and cortisol response to opioid receptor blockade induced by naloxone hydrochloride compared with FHN subjects. | |||||||||||||||
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Selective blockade of excitatory opioid receptor functions by low (ca. pM) concentrations of naloxone, naltrexone, etorphine and other specific agents markedly increases the inhibitory potency of morphine or other bimodally acting agonists and attenuates development of tolerance/dependence. | |||||||||||||||
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This study was designed to evaluate ACTH responses to opioid receptor blockade as a function of family history for alcohol dependence. | |||||||||||||||
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General Comments
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