INT90743
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
The opioid receptor antagonist naloxone completely blocked morphine induction of GPDH but had no effect on GPDH induction by noxious heat stimulation or metamizol treatment, implicating different mechanisms of GPDH induction. | |||||||||||||||
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The opioid receptor antagonist naloxone completely blocked morphine induction of GPDH but had no effect on GPDH induction by noxious heat stimulation or metamizol treatment, implicating different mechanisms of GPDH induction. | |||||||||||||||
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Surprisingly, administration of analgesic doses of morphine or the nonsteroidal antiinflammatory drugs aspirin, metamizol (dipyrone), and indomethacin also increased GPDH mRNA levels in rat spinal cord. | |||||||||||||||
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Nevertheless, in all cases, induction of the GPDH gene requires adrenal steroids and new protein synthesis, as the induction was blocked in adrenalectomized rats and by cycloheximide treatment, respectively. | |||||||||||||||
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Northern blot and in situ hybridization analysis confirmed the differential display results; they also showed, in a separate model of neuronal activation, that after thermal noxious stimulation of the hind-paws, a similar increase in GPDH mRNA occurs in the areas of somatotopic projection in the lumbar spinal cord. | |||||||||||||||
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Our results suggest that the induction of the GPDH gene upon peripheral noxious stimulation is related to the endogenous response to pain as it is mimicked by exogenously applied analgesic drugs. | |||||||||||||||
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The transcriptional upregulation of glycerol-3-phosphate dehydrogenase 1 (Gpd1) and FK506-binding protein (Fkbp51) mRNA (Table 4, Figure 4) indicate: 1) that pyrethroid exposure activates the hypothalamic-pituitary-adrenal (HPA) axis and 2) that non-neuronal cell populations in the CNS are sensitive to pyrethroids. | |||||||||||||||
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The potential impact of increased Gpd1 and Fkbp51 expression on the health and function of affected glia, to date, is unclear. | |||||||||||||||
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For deltamethrin, both Camk1g and Gpd1 mRNA had maximally induced expression at 3 h followed by persistent elevations at 6 h (Figure 4). | |||||||||||||||
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The opioid receptor antagonist naloxone completely blocked morphine induction of GPDH but had no effect on GPDH induction by noxious heat stimulation or metamizol treatment, implicating different mechanisms of GPDH induction. | |||||||||||||||
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Using mRNA differential display, we found that the gene for NAD(+)-dependent glycerol phosphate dehydrogenase (GPDH; EC 1.1.1.8) is induced in rat brain following seizure activity. | |||||||||||||||
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For permethrin, both Camk1g and Gpd1 had maximal induction at 6 h preceded by slight elevations at 3 h. | |||||||||||||||
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Permethrin-mediated Gpd1 induction was statistically significant while Camk1g induction reflected the trends observed in the dose-response cohorts but did not reach statistical significance. | |||||||||||||||
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