INT29105
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Preclinical studies suggest that visceral afferents constitutively express kappa-opioid receptors (KORs) and that noxious visceral stimuli can be inhibited at a peripheral site by KOR activation. | |||||||||||||||
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These findings are consistent with complex consequences of KOR activation in the spinal cord. | |||||||||||||||
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These findings demonstrate for the first time that kappa2 receptor numbers are upregulated by cocaine exposure. | |||||||||||||||
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These results suggest that select opioid ligands up-regulate rKOR by enhancing the rate of receptor folding and maturation and by protecting the receptor from degradation, resulting in an increase in the number of rKOR binding sites, immunoreactive protein, and functional receptors. | |||||||||||||||
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KOR activation by its endogenous ligand dynorphin A(1-17) decreases basal and drug-induced striatal levels of dopamine. | |||||||||||||||
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Estrogen and progesterone activate spinal kappa-opiate receptor analgesic mechanisms. | |||||||||||||||
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This indicates that exposure (of non-pregnant animals) to the pregnancy blood profile of E2 and P activates a spinal cord kappa-opiate receptor analgesic system, as occurs during actual gestation. | |||||||||||||||
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A select set of opioid ligands induce up-regulation by promoting the maturation and stability of the rat kappa-opioid receptor in human embryonic kidney 293 cells. | |||||||||||||||
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Emphasis will be placed on demonstration of a rodent model in which butorphanol administration induces dependence through a unique (in comparison with morphine) activation of the kappa-opioid receptor. | |||||||||||||||
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Pan discusses the accumulating evidence that activation of the kappa-receptor antagonizes various mu-receptor-mediated actions in the brain, including analgesia, tolerance, reward and memory processes. | |||||||||||||||
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Various parameters governing the arterial baroreflex control of heart rate were assessed before and after activation of kappa-opiate receptors (KOR) by i.v. administration of the specific KOR agonist U-50488H (experiment 1) or vehicle (experiment 2) to conscious, chronically instrumented lambs aged 42 +/- 2 days (n = 6). | |||||||||||||||
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These results suggest that select opioid ligands up-regulate rKOR by enhancing the rate of receptor folding and maturation and by protecting the receptor from degradation, resulting in an increase in the number of rKOR binding sites, immunoreactive protein, and functional receptors. | |||||||||||||||
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CONCLUSIONS: Our results demonstrate that expression of three types of ORs, MOR, DOR and KOR, was markedly upregulated in human hypertrophic scars, suggesting a possible link between upregulated ORs and local cacaesthesia in hypertrophic scars.
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Thus, the high affinity that buprenorphine has for the kappa receptor results in potent kappa receptor antagonist activity in vivo. | |||||||||||||||
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Related studies focused on full-length cloning of the coding region of the rhesus monkey kappa-opioid receptor (OPRK1) gene and revealed a high homology of the nonhuman primate OPRK1 gene compared with the human OPRK1 gene, including particular C-terminal residues thought to be involved in receptor desensitization and internalization. | |||||||||||||||
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In addition, the presence of increased KOR density and proportionally elevated intracellular KORs in proestrus/estrus females suggests a basis for sex-linked differences in KOR-mediated antinociception. | |||||||||||||||
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The data confirm the participation of glutamate as a general phenomenon in opioid dependence, identify the locus coeruleus as a primary site for glutamatergic mediation of dependence, and suggest novel aspects to the neuropharmacology of opioid dependence with respect to the role of the kappa-opioid receptor. | |||||||||||||||
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Brefeldin A caused accumulation of intracellular rKOR intermediates, and coincubation with naltrexone increased the levels of the brefeldin-induced species significantly. | |||||||||||||||
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Naltrexone did not alter rKOR mRNA levels or translational efficiency, and rKOR up-regulation was not inhibited by cycloheximide. | |||||||||||||||
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The present study further demonstrates that the KOR of lymphocytes are activated in the presence of extracellular morphine or U50,488H, a KOR selective agonist, and the activation causes an increase in the expression of KOR mRNA, as determined by a quantitative competitive Reverse Transcriptase-Polymerase Chain Reaction (RT-PCR) procedure. | |||||||||||||||
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