Molecular mechanisms in dizocilpine-induced attenuation of development of morphine dependence: an association with cortical Ca2+/calmodulin-dependent signal cascade

Hamdy, Moustafa Mahmoud; Noda, Yukihiro; Miyazaki, Masaru; Mamiya, Takayoshi; Nozaki, Ayumu; Nitta, Atsumi; Sayed, Merfat; Assi, Abdel-Azim; Gomaa, Adel A.; Nabeshima, Toshitaka

doi:10.1016/j.bbr.2003.10.014

Cited by 19 publications

(19 citation statements)

References 26 publications

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“…Trujillo and Akil (1994) subsequently demonstrated that the effect was shared by other noncompetitive NMDA antagonists, including ketamine, dextrorphan, and phencyclidine. The ability of NMDA antagonists to prevent the development of tolerance and dependence in rodents also has been shown by several other investigators (e.g., Elliott et al 1994;Hamdy et al 2004;Mao et al 1996;Popik and Skolnick 1996;Tiseo and Inturrisi 1993;Tiseo et al 1994).…”

Section: Introductionmentioning

confidence: 85%

Memantine produces modest reductions in heroin-induced subjective responses in human research volunteers

Comer

Sullivan

2007

Psychopharmacology

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Section: Introductionmentioning

confidence: 85%

Memantine produces modest reductions in heroin-induced subjective responses in human research volunteers

Comer

Sullivan

2007

Psychopharmacology

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“…39 However, to efficiently block NMDA receptors, naloxone had to be used in high (300 mM) concentrations, whereas plasma naloxone concentrations only reached low micromolar values in in vivo studies similar to our experimental settings. 40,41 Moreover, it is unlikely that naloxone may have a direct effect on the NMDA receptor at the currently administered dose, as NMDA receptor antagonism is related to anti-nociception and prevention of withdrawal, 41,42 which are opposite to the naloxone-precipitated effects. Naloxone also proved to reverse neuropathic pain in rats via inhibition of toll-like receptor 4 (TLR4) signaling.…”

mentioning

confidence: 96%

Effect of Subchronic Intravenous Morphine Infusion and Naloxone-Precipitated Morphine Withdrawal on P-gp and Bcrp at the Rat Blood–Brain Barrier

Chaves

Gómez-Zepeda

Auvity

et al. 2016

Journal of Pharmaceutical Sciences

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“…Thus, the reversal of tolerance would be mediated by the same mechanism as indicated previously for noncompetitive NMDA receptor antagonists (Trujillo and Akil, 1991). It was reported that selective NMDA receptor antagonists attenuated the development of morphine tolerance (Hamdy et al, 2004;Danysz et al, 2005). Stimulation of NMDA receptors was shown to disinhibit GSK3␤ by PPI-mediated dephosphorylation of GSK3␤ at the Ser 9 (Szatmari et al, 2005).…”

mentioning

confidence: 65%

Effects of Glycogen Synthase Kinase 3β and Cyclin-Dependent Kinase 5 Inhibitors on Morphine-Induced Analgesia and Tolerance in Rats

Parkitna

Obara²,

Wawrzczak-Bargieła³

et al. 2006

J Pharmacol Exp Ther

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Repeated administration of morphine is associated with the development of tolerance, yet the mechanism underlying this phenomenon is still poorly understood. Recent evidence implicating glycogen synthase kinase 3 (GSK3) in opioid receptor signaling pathways has prompted us to investigate its role in morphine tolerance. Administration of 10 mg/kg morphine i.p. to Wistar rats twice daily for 8 days resulted in complete tolerance to its analgesic effects as measured by the tail-flick test. When injections of morphine were preceded by intrathecal (i.t.) administration of either an inhibitor of GSK3 [(3-(2,4-dichlorophenyl)-4-(1-methyl-1H-indol-3-yl)-1H-pyrrole-2,5-dione (SB216763) or 6-bromoindirubin-3Јoxime] or an inhibitor of cyclin-dependent kinase (Cdk), roscovitine, development of tolerance to morphine analgesia was completely abolished. In addition, a single i.t. injection of either kinase inhibitor was able to restore in a dose-dependent manner the analgesic effect of morphine in morphine-tolerant rats. None of the inhibitors in doses used in the present study had analgesic effects of their own nor an effect on the analgesic potency of morphine. Repeated i.t. administration of either inhibitor had caused an increase in abundance of GSK-3␤ phosphorylated at Ser 9 in the dorsal lumbar part of the spinal cord of rats that were chronically treated with morphine. Furthermore, reversal of morphine tolerance by a single injection of either inhibitor was always associated with increased abundance of phospho-GSK3␤. In conclusion, our data indicate that chronic morphine treatment activates a highly efficient pathway by means of which Cdk5 regulates GSK3␤ activity.Adaptations in cellular signaling evoked by repeated morphine administration that lead to development of tolerance are still unclear. Binding of morphine to its main target, the -opioid receptor, results in the activation of a G i/o protein, inhibition of adenylate cyclases, and downregulation of the cAMP second messenger pathway. Prolonged exposure to morphine or specific -opioid receptor agonists has an opposite effect and leads to up-regulation of the cAMP pathway, possibly through the actions of the ␤␥ subunits of G i/o proteins (Tan et al., 2003), although the involvement of regulators of G protein signaling (RGS proteins) was also indicated (Gold et al., 2003). It was reported that morphine could activate the mitogen-activated protein kinase cascade (Berhow et al., 1996;Bohn et al., 2000;Bilecki et al., 2004;Muller and Unterwald, 2004) with the involvement of the phosphoinositol-3-kinase and protein kinase C kinases (Tan et al., 2003;Belcheva et al., 2005). Activation of the phosphoinositol-3-kinase also led to phosphorylation of Akt and other down-stream effectors (Polakiewicz et al., 1998;Iglesias et al., 2003;Muller and Unterwald, 2004). Recent evidence points to the possibil-

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Molecular mechanisms in dizocilpine-induced attenuation of development of morphine dependence: an association with cortical Ca2+/calmodulin-dependent signal cascade

Cited by 19 publications

References 26 publications

Memantine produces modest reductions in heroin-induced subjective responses in human research volunteers

Memantine produces modest reductions in heroin-induced subjective responses in human research volunteers

Effect of Subchronic Intravenous Morphine Infusion and Naloxone-Precipitated Morphine Withdrawal on P-gp and Bcrp at the Rat Blood–Brain Barrier

Effects of Glycogen Synthase Kinase 3β and Cyclin-Dependent Kinase 5 Inhibitors on Morphine-Induced Analgesia and Tolerance in Rats

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