Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transient thermal, but not mechanical, hypoalgesia appears at the early stages of the development of an hyperalgesic murine osteosarcoma. This hypoalgesia is suppressed by the administration of naloxone, its peripherally acting analog naloxone methiodide, the mu- and delta-opioid receptor antagonists cyprodime and naltrindole, or the CRF receptor antagonist, alpha-helical CRF (9-41). When immunohistochemical assays were performed with an anti-beta-endorphin antibody, whose in vivo administration suppressed the analgesia, labeled mononuclear immune cells appeared both inside and surrounding the tumoral tissue. In conclusion, the peripheral action of beta-endorphin, released in response to the osteosarcoma seems responsible for the observed thermal analgesia.
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PMID:Endogenous beta-endorphin induces thermal analgesia at the initial stages of a murine osteosarcoma. 1693 Jul 72

Tolerance to peripheral antinociception after chronic exposure to systemic morphine was assessed in mice with chronic CFA-inflammation; cross-tolerance to locally administered mu, delta and kappa-opioid agonists and levels of beta-arrestins in the injured paw, were also evaluated. Tolerance was induced by the subcutaneous implantation of a 75 mg morphine-pellet, and antinociception evaluated with the Randall-Selitto test, 5 min after the subplantar injection of morphine, fentanyl, buprenorphine, DPDPE, U-50488H or CRF. Experiments were performed in the absence and presence of CFA-inflammation, in animals implanted with a morphine or placebo pellet. Beta-arrestin protein levels were determined by western blot. In mice without inflammation, subplantar opioids did not induce antinociception, while during CFA-inflammation, all drugs generated dose-response curves with an order of potency of: U-50488H < DPDPE < morphine < buprenorphine < fentanyl << CRF. During CFA-inflammation plus morphine-pellet, the potency of fentanyl decreased 1.25 times, while that of DPDPE, U-50488H and CRF diminished approximately 2.5-4.3 times. For each drug, the ratio between the ED(50)'s in tolerant and naive animals, was significantly higher than 1 (except for buprenorphine and fentanyl), demonstrating partial cross-tolerance to systemic morphine. Inflammation induced a twofold increase in beta-arrestin expression (p<0.01), and the levels decreased after acute morphine exposure (p<0.05). Tolerance did not alter beta-arrestins, but partially prevented the increase induced by inflammation. The results suggest that peripheral beta-arrestins could facilitate peripheral OR-desensitization and tolerance development. Clinically, the experiments could be useful to establish the effectiveness of local opioid administration in patients with musculoskeletal pain, chronically receiving morphine analgesia.
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PMID:Tolerance to the antinociceptive effects of peripherally administered opioids. Expression of beta-arrestins. 1902 93

The aim of this study was to investigate the participation of glucocorticoid receptors and corticotropin releasing factor receptors of subtype 2 (CRF-2 receptors) in the analgesic effect of CRF on somatic pain sensitivity. The participation of glucocorticoid receptors and CRF-2 receptors in the CRF-induced analgesia was investigated by the receptors antagonists: RU38486 or astressin 2-B, respectively, in anaesthetized rats. For estimation of pain sensitivity the threshold of pain reaction induced by electrical stimulation of the rat' tail as tested before and during 30 min after the systemic injection of CRF. The CRF-induced analgesic effect was partly abolished by glucocorticoid receptor antagonist RU 38486 and completely abolished by CRF-2 receptor antagonist astressin 2-B. The data suggest that glucocorticoid receptors and CRF-2 receptors participate in the CRF-induced analgesic effect.
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PMID:[Analgesic effect of corticotropin releasing factor (CRF) on somatic pain sensitivity: participation of glucocorticoid and CRF-2 receptors]. 1906 25

The aim of the present work was to study the involvement of glucocorticoid receptors and corticotropin-releasing factor type 2 receptors (CRF-2 receptors) in mediating the analgesic effects of CRF on somatic pain sensitivity. The involvement of glucocorticoid and CRF-2 receptors in the development of analgesia evoked by systemic administration of CRF was studied by blockade of these receptors by their specific antagonists RU 38486 and astressin 2-B, respectively, in anesthetized rats. Pain sensitivity was tested before and 30 min after administration of CRF in terms of the threshold of the pain reaction induced by stimulation of the rat's tail with an electric current. Blockade of glucocorticoid receptors induced partial suppression of the analgesic action of CRF, while blockade of CRF-2 receptors produced complete suppression of the analgesic effect. These results provide evidence that glucocorticoid and CRF-2 receptors are involved in mediating the analgesic effects of CRF.
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PMID:Analgesic actions of corticotropin-releasing factor (CRF) on somatic pain sensitivity: involvement of glucocorticoid and CRF-2 receptors. 1983 May 68


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