INT6067
From wiki-pain
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Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
NGF treatment of PC12h cells also results in the induction of delta opioid receptor (DOR-1) mRNA. | |||||||||||||||
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NGF treatment of PC12h cells also results in the induction of delta opioid receptor (DOR-1) mRNA. | |||||||||||||||
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The results show that opioid receptor activation in the LPBN induces hypertonic sodium intake in satiated and normohydrated rats, an effect not due to general ingestive behavior facilitation. | |||||||||||||||
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These results provide evidence that naltrex-one-induced upregulation of the opioid receptor complex might occur indirectly as a consequence of interactions at beta-funaltrexamine-insensitive opioid receptors and that morphine-induced upregulation (increased Bmax) of the opioid receptor complex is a relevant in vitro marker related to the development of tolerance and dependence. | |||||||||||||||
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These results provide evidence that naltrex-one-induced upregulation of the opioid receptor complex might occur indirectly as a consequence of interactions at beta-funaltrexamine-insensitive opioid receptors and that morphine-induced upregulation (increased Bmax) of the opioid receptor complex is a relevant in vitro marker related to the development of tolerance and dependence. | |||||||||||||||
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These results provide evidence that naltrex-one-induced upregulation of the opioid receptor complex might occur indirectly as a consequence of interactions at beta-funaltrexamine-insensitive opioid receptors and that morphine-induced upregulation (increased Bmax) of the opioid receptor complex is a relevant in vitro marker related to the development of tolerance and dependence. | |||||||||||||||
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Both peptides concentration dependently (1 nM-1 microM) inhibited the release of radiolabeled acetylcholine (ACh) from striatal slices (pD2 7.6-7.9), an effect exclusively mediated by delta-opioid receptor activation. | |||||||||||||||
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Therefore, the purpose of the present study was to test the hypothesis that ischemia- and morphine-induced cardioprotection are mediated via stimulation of the delta-opioid receptor in the rat heart. | |||||||||||||||
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Although it is still unclear about the cellular and molecular mechanisms of morphine analgesia, evidence supported that morphine-induced opioid-receptor activation results in the enhancement of phosphorylation of mitogen-activated protein kinase (MAPK) in ACC, SI and locus ceruleus [38]. | |||||||||||||||
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On the contrary, activation of both mu- or delta-opioid receptors in the ventral tegmental area significantly increased self-stimulation and decreased spontaneous motor activity, supporting the view that different mechanisms underlie the behavioural effects, resulting from enhancement of endogenous enkephalins and from activation of specific opioid receptors in the ventral mesencephalon. | |||||||||||||||
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The antihyperalgesic potency of the mu opioid receptor agonist [D-Ala(2),N-Me-Phe(4),Gly(5)-ol]enkephalin (DAMGO), determined for the inflamed hindpaw, was enhanced 4 d and 2 weeks after injury. | |||||||||||||||
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Furthermore, both DSTBULET and BUBU caused a strong inhibition (pD2 8.2-8.3) of D-1 dopamine receptor-stimulated cyclic AMP efflux from striatal slices, an effect known to be mediated by mu- and/or delta-opioid receptor activation. | |||||||||||||||
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The interactions between dopamine receptors and opioid receptors coupled to adenylate cyclase in rat neostriatum were investigated. cAMP efflux from neostriatal slices induced by simultaneous activation of (stimulatory) D-1 and (inhibitory) D-2 dopamine receptors with 30 microM dopamine was inhibited by the preferential delta-opioid receptor agonist [D-Ala2-D-Leu5] enkephalin (DADLE) and the mu-opioid receptor agonist morphine with an EC50 of 100 and 800 nM, respectively. | |||||||||||||||
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Inflammation and hyperalgesia induce a dramatic up-regulation of opioid messenger RNA and peptide levels in nociceptive neurons of the spinal dorsal horn. | |||||||||||||||
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This finding is contradictory to the generally held view that antagonist-induced opioid receptor up-regulation in brain increases asymptotically, leveling off after a relatively brief treatment period. | |||||||||||||||
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These results clearly indicate that activation of the mu opioid receptor increases the number of spike-wave discharges, and that modulation of delta receptors is not effective. | |||||||||||||||
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PERSPECTIVE: Although the role of adenosine release in the spinal cord for opioid receptor activation in subsequent analgesia from opioids is controversial in laboratory studies, these clinical data suggest that local opioid receptor stimulation in the spinal cord of humans does release adenosine. | |||||||||||||||
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An alternative hypothesis is that opioid receptors remain operative following repeated opiate administration but that opioid receptor activation rapidly induces a prolonged increase in pain sensitivity which opposes the predominant opiate analgesic effect following repeated opiate administration. | |||||||||||||||
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Chronic fentanyl treatments induce the up-regulation of mu opioid receptor mRNA in rat pheochromocytoma cells. | |||||||||||||||
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These results indicate that vasodilator responses to TAPP and endomorphin 2 are mediated by the activation of a naloxone-sensitive opioid receptor and the release of nitric oxide from the endothelium within the hindquarter vascular bed of the rat. | |||||||||||||||
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General Comments
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