Aquaporin 4 deficiency modulates morphine pharmacological actions

Wu, Ning; Lü, Xin; Yan, Hang; Su, Rui‐Bin; Wang, Jifang; Yin, Liu; Hu, Gang; Jin, Li

doi:10.1016/j.neulet.2008.10.065

Cited by 39 publications

(31 citation statements)

References 30 publications

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“…It is noteworthy that altered glutamate homeostasis due to decreased glial glutamate transporter expression has been demonstrated in several CNS disturbances in which glia assume a reactive phenotype (Tilleux and Hermans, 2007). Long-term morphine administration results in an elevation of cerebrospinal fluid levels of aspartate and glutamate (Wen et al, 2005;Tai et al, 2007;Wu et al, 2008), most likely resulting from down-regulation of glial GLT-1 and GLAST glutamate transporters (Ozawa et al, 2001;Mao et Tai et al, 2006Tai et al, , 2007Lin et al, 2010a;Rawls et al, 2010). This elevation of aspartate and glutamate seems to involve aquaporin 4 and is sensitive to coadministration with dexamethasone (Wen et al, 2005), ceftriaxone (Rawls et al, 2010), naloxone (Mao et al, 2002), and amitriptyline (Tai et al, 2006(Tai et al, , 2007.…”

Section: Opioid-induced Changes In Non-neuronal Cells Contribute To Tmentioning

confidence: 99%

“…Another critical modulation in glial function related to opioid-induced central immune signaling that contributes to the development of tolerance is down-regulation of glial GLT-1 and GLAST glutamate transporters (Ozawa et al, 2001;Mao et al, 2002;Nakagawa and Satoh, 2004;Wen et al, 2005;Tai et al, 2006Tai et al, , 2007Wu et al, 2008;Lin et al, 2010a;Rawls et al, 2010). The effects of such down-regulation are blocked by coadministration of any of the following substances: synthetic glucocorticoid dexamethasone (Wen et al, 2005); the glutamate transporter up-regulator ceftriaxone (Rawls et al, 2010); (Ϫ)-naloxone (Mao et al, 2002); ultra-lowdose naloxone (Lin et al, 2010a); or amitriptyline, which produces its effect via induction of IL-10 expression and hence indirect induction of an anti-inflammatory response (Tai et al, 2006(Tai et al, , 2007.…”

Section: What Is the Impact Of Proinflammatory Central Immune Signmentioning

confidence: 99%

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Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Hutchinson

Shavit

Grace³

et al. 2011

Pharmacol Rev

343

315

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Section: Opioid-induced Changes In Non-neuronal Cells Contribute To Tmentioning

confidence: 99%

Section: What Is the Impact Of Proinflammatory Central Immune Signmentioning

confidence: 99%

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Hutchinson

Shavit

Grace³

et al. 2011

Pharmacol Rev

343

315

View full text Add to dashboard Cite

“…The dosage regimen www.nature.com/aps Wen Q et al Acta Pharmacologica Sinica npg was used for the induction of drug tolerance, as previously reported by our laboratory [27] . The antinociceptive effects were measured 30 min after administration of the opioid drugs every day to monitor the development of tolerance.…”

Section: Dosage Regimen and Injection Procedures In Thermal Nociceptionmentioning

confidence: 99%

“…Many previous studies have used high doses of opioid drugs to induce and study tolerance [27,30,31] . As expected, repeated treatment with morphine (30 mg/kg, sc, thrice daily) induced the rapid development of analgesic tolerance.…”

Section: Development Of 030418 Tolerance and The Effect Of Pretreatmementioning

confidence: 99%

Pharmacological mechanisms underlying the antinociceptive and tolerance effects of the 6,14-bridged oripavine compound 030418

Wen¹,

Yu²,

Li³

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate possible pharmacological mechanisms underlying the antinociceptive effect of and tolerance to N-methyl-7α-[(R)-1-hydroxy-1-methyl-3-(thien-3-yl)-propyl]-6,14-endo-ethanotetrahydronororipavine (030418), a derivative of thienorphine. Methods: The binding affinity and efficacy of 030418 were determined using receptor binding and guanosine 5′-O-(3-[ 35 S]thio)triphosphate ([ 35 S]GTPγS) assays in CHO-μ, CHO-κ, CHO-δ, and CHO-ORL1 cell membranes. The analgesic activity of and tolerance to 030418 were evaluated in thermal nociceptive tests in mice. The effects of 030418 on opioid receptors were further investigated using in vivo pharmacological antagonist blockade and in vitro tissue preparations. Results: The compound 030418 displayed high binding affinity to all subtypes of opioid receptors with K i values in the nanomolar range. In [ 35 S]GTPγS binding assay, the maximal stimulation of 030418 to μ-, κ-, δ-receptors and the ORL1 receptor was 89%, 86%, 67% and 91%, respectively. In hot-plate test, the antinociceptive effect of 030418 was more potent and longer than morphine. The nonselective opioid receptor antagonist naloxone could completely block 030418-induced antinociception, while both the μ-opioid receptor antagonist β-FNA and the κ-opioid receptor antagonist nor-BNI attenuated 030418-induced antinociception. In contrast, the ORL1 receptor antagonist J-113397 enhanced the antinociceptive effect of 030418. Additionally, chronic treatment with 030418 resulted in a dramatic development of tolerance that could not be effectively prevented by J-113397. In guinea pig ileum preparation, the existing action of 030418 could be removed with difficulty after prolonged washing. Conclusion:The compound 030418 is a novel agonist of opioid receptors with high efficiency, long-lasting effect and liability to tolerance, which may be closely correlated with the methyl group at the N 17 position and the high hydrophobicity of the C 7 -thiophene group in its chemical structure.

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“…Recent studies showed that AQP4 deficiency potentiated morphine analgesia but attenuated chronic morphineinduced tolerance in hot-plate test (Wu et al 2008). However, the role of spinal AQP4 in morphine analgesia and tolerance remains unknown.…”

Section: Introductionmentioning

confidence: 99%

Effects of Aquaporin 4 Deficiency on Morphine Analgesia and Chronic Tolerance: A Study at Spinal Level

2010

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Recent reports showed that aquaporin 4 (AQP4) deficiency potentiated morphine analgesia but attenuated chronic morphine-induced tolerance in hot-plate test, predominantly reflecting supraspinal pain response. The present study investigated the effects of AQP4 deficiency on morphine analgesia and tolerance using tail flick test, primarily reflecting spinal response. It was found that (1) chronic morphine treatment resulted in decreased expression of spinal AQP4 in mice detected by Western blotting analysis; (2) in tail flick test, AQP4 knockout mice displayed significant impaired morphine analgesia without influencing the progress of chronic tolerance; and (3) the expressions of mu-opioid receptor (MuOR) and glutamate transporter 1 (GLT-1) in AQP4 knockout mice spinal cord were lower than those in wild-type mice, whereas chronic morphine-induced alteration characteristics of spinal MuOR or GLT-1 expression were not affected by AQP4 deficiency. In conclusion, AQP4 deficiency attenuated morphine acute antinociception but did not affect chronic tolerance in tail flick test, implying a role for spinal AQP4 in morphine analgesia but not in chronic tolerance.

show abstract

Aquaporin 4 deficiency modulates morphine pharmacological actions

Cited by 39 publications

References 30 publications

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Exploring the Neuroimmunopharmacology of Opioids: An Integrative Review of Mechanisms of Central Immune Signaling and Their Implications for Opioid Analgesia

Pharmacological mechanisms underlying the antinociceptive and tolerance effects of the 6,14-bridged oripavine compound 030418

Effects of Aquaporin 4 Deficiency on Morphine Analgesia and Chronic Tolerance: A Study at Spinal Level

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