INT31393
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
However, recent studies suggest that short term morphine pretreatment can increase delta opioid receptor-mediated antinociception by promoting the translocation of delta opioid receptor to the cell surface. | |||||||||||||||
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Dopamine antagonists increased opioid action, an action that may depend more on the increased release of endogenous opioids than on supersensitivity of the opioid receptor. | |||||||||||||||
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Juvenile isolation increased general activity during the social interaction test, an effect which was accompanied by a reduction of opioid receptor occupancy in many brain areas, suggesting an increased opioid peptide release as a consequence of socially-induced general activity. | |||||||||||||||
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Morphine treatment in isolated rats caused an increase in adult social activity and enhanced opioid peptide release in some cortical regions and the ventral tegmental area as compared to saline treated rats. | |||||||||||||||
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Potassium ions also caused an increase, followed by a decrease, in opioid peptide release, and naloxone also prevented the latter from occurring. | |||||||||||||||
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Potassium ions also caused an increase, followed by a decrease, in opioid peptide release, and naloxone also prevented the latter from occurring. | |||||||||||||||
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Delta(2)-opioid receptor mediation of morphine-induced CCK release in the frontal cortex of the freely moving rat. | |||||||||||||||
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Ventral tegmental self-stimulation selectively induces opioid peptide release in rat CNS. | |||||||||||||||
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Elevation of intracellular Ca2+ is required for opioid peptide release [17]. | |||||||||||||||
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Opioid peptide release requires a stimulus such as cold water swim [43] or intraplantar injection of corticotrophin releasing hormone, cytokines (e.g. interleukin-1) [44] or chemokines (CXCL2/3) [17],[18]. | |||||||||||||||
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Mycobacteria or bacterial products may trigger opioid peptide release in arthritic joints or at the site of surgery with accompanying infection. | |||||||||||||||
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In line with the lack of opioid peptide release after TLR-2 or TLR-4 stimulation, the Mycobacterium butyricum-induced release of Met-enkephalin could not be blocked by single or combined TLR-2/4 blockade (Fig. 6A, 7B). | |||||||||||||||
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In line with the lack of opioid peptide release after TLR-2 or TLR-4 stimulation, the Mycobacterium butyricum-induced release of Met-enkephalin could not be blocked by single or combined TLR-2/4 blockade (Fig. 6A, 7B). | |||||||||||||||
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We further examined the role of TLR and FPR in mycobacterial stimulation of opioid peptide release. | |||||||||||||||
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We found that Mycobacterium butyricum induced opioid peptide release from neutrophils through FPR but not TLR stimulation. | |||||||||||||||
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In this study we examined whether heat inactivated Mycobacterium butyricum triggers opioid peptide release from rat and human neutrophils and monocytes and whether this requires FPR and/or TLR activation. | |||||||||||||||
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We hypothesized that Mycobacterium butyricum might directly trigger opioid peptide release. | |||||||||||||||
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Mycobacteria can trigger opioid peptide release from neutrophils but not from monocytes | |||||||||||||||
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In vitro, heat inactivated Mycobacterium butyricum triggers opioid peptide release from neutrophils, but not from monocytes. | |||||||||||||||
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Alternatively, other releasing agents such as chemokines (CXCR1/2 ligands) can trigger opioid peptide release from rat and human neutrophils [17],[18] and these are produced in complete Freund's adjuvant-induced inflammation [14] as well as in surgical wounds [69].
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General Comments
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