Are NMDA receptors involved in opiate-induced neural and behavioral plasticity?

Trujillo, Keith A.

doi:10.1007/s002130000416

Cited by 126 publications

(108 citation statements)

References 166 publications

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“…Although there is little evidence that glycine A receptors participate in morphine addiction, it is well understood that NMDA receptor antagonists, including drugs that block glycine B receptors, produce a pharmacological profile in tests of morphine place preference, tolerance, dependence, and withdrawal similar to what is shown here for Gly-Gln (Kolesnikov et al, 1994;Trujillo, 2000;Ossipov et al, 2004). To initially assess the possibility that Gly-Gln inhibits morphine withdrawal by blocking glycine B receptors, we tested whether D-serine, a glycine B receptor agonist (Witkin et al, 1997), would prevent Gly-Gln from suppressing morphine withdrawal symptoms.…”

supporting

confidence: 62%

Glycyl-Glutamine, an Endogenous β-Endorphin-Derived Peptide, Inhibits Morphine-Induced Conditioned Place Preference, Tolerance, Dependence, and Withdrawal

Çavun

Göktalay²,

Millington³

2005

J Pharmacol Exp Ther

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Glycyl-glutamine (Gly-Gln; ␤-endorphin [30][31] ) is an endogenous dipeptide synthesized from ␤-endorphin 1-31 . Previous investigations have shown that Gly-Gln inhibits the cardiovascular and respiratory depression caused by morphine and ␤-endorphin 1-31 , but it does not interfere with opioid analgesia. In this study, we tested whether Gly-Gln administration would influence morphine-induced conditioned place preference, tolerance, dependence, or withdrawal. For place preference experiments, rats were conditioned with morphine sulfate (2.5 mg/kg i.p.) or saline on alternate days for 6 days and tested on day 7. Glycyl-glutamine (1-100 nmol i.c.v.) pretreatment inhibited acquisition of a conditioned place preference to morphine significantly. Glycyl-glutamine (100 nmol i.c.v.) also blocked expression of a pre-established morphine place preference, but it did not interfere with acquisition of a conditioned place preference to palatable food, and it did not produce place preference or aversion when given alone to morphine-naive animals. To induce antinociceptive tolerance, rats were treated with morphine (10 mg/kg i.p.) twice daily for 7 days, and morphine antinociception was evaluated with the tail-flick test. Glycylglutamine (100 nmol i.c.v.) pretreatment delayed the onset of morphine tolerance significantly and partially reversed pre-established tolerance. Morphine dependence and withdrawal were assessed by measuring naloxone-precipitated withdrawal symptoms. Glycyl-glutamine inhibited the development of morphine dependence when given to rats twice daily immediately before they received morphine (10 mg/kg i.p.) and suppressed withdrawal symptoms of rats with subcutaneously implanted morphine pellets when administered 5 min before withdrawal was induced with naloxone. Glycyl-glutamine thus attenuates morphine-induced conditioned place preference, tolerance, dependence, and withdrawal without compromising morphine analgesia.

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supporting

confidence: 62%

Glycyl-Glutamine, an Endogenous β-Endorphin-Derived Peptide, Inhibits Morphine-Induced Conditioned Place Preference, Tolerance, Dependence, and Withdrawal

Çavun

Göktalay²,

Millington³

2005

J Pharmacol Exp Ther

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“…Tolerance to the analgesic effect of opioids can be readily observed in animal pain models (for review, see Trujillo, 2000) and can also occur in the clinical setting, necessitating dose increases during prolonged treatment (Ballantyne and Mao, 2003). Tolerance development to the analgesic effect of tapentadol in the CCI model in rats during repeated administration was much delayed compared with morphine.…”

Section: Discussionmentioning

confidence: 99%

(–)-(1R,2R)-3-(3-Dimethylamino-1-ethyl-2-methyl-propyl)-phenol Hydrochloride (Tapentadol HCl): a Novel μ-Opioid Receptor Agonist/Norepinephrine Reuptake Inhibitor with Broad-Spectrum Analgesic Properties

Tzschentke

Christoph²,

Kögel³

et al. 2007

J Pharmacol Exp Ther

370

389

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ABSTRACT(Ϫ)-(1R,2R)-3-(3-Dimethylamino-1-ethyl-2-methyl-propyl)-phenol hydrochloride (tapentadol HCl) is a novel -opioid receptor (MOR) agonist (K i ϭ 0.1 M; relative efficacy compared with morphine 88% in a [35 S]guanosine 5Ј-3-O-(thio)triphosphate binding assay) and NE reuptake inhibitor (K i ϭ 0.5 M for synaptosomal reuptake inhibition). In vivo intracerebral microdialysis showed that tapentadol, in contrast to morphine, produces large increases in extracellular levels of NE (ϩ450% at 10 mg/kg i.p.). Tapentadol exhibited analgesic effects in a wide range of animal models of acute and chronic pain [hot plate, tail-flick, writhing, Randall-Selitto, mustard oil colitis, chronic constriction injury (CCI), and spinal nerve ligation (SNL)], with ED 50 values ranging from 8.2 to 13 mg/kg after i.p. administration in rats. Despite a 50-fold lower binding affinity to MOR, the analgesic potency of tapentadol was only two to three times lower than that of morphine, suggesting that the dual mode of action of tapentadol may result in an opiate-sparing effect. A role of NE in the analgesic efficacy of tapentadol was directly demonstrated in the SNL model, where the analgesic effect of tapentadol was strongly reduced by the ␣ 2 -adrenoceptor antagonist yohimbine but only moderately attenuated by the MOR antagonist naloxone, whereas the opposite was seen for morphine. Tolerance development to the analgesic effect of tapentadol in the CCI model was twice as slow as that of morphine. It is suggested that the broad analgesic profile of tapentadol and its relative resistance to tolerance development may be due to a dual mode of action consisting of both MOR activation and NE reuptake inhibition.

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“…Ionotropic glutamate receptors in the VTA modulate opiate reinforcement (Xi and Stein, 2002). Moreover, NMDA receptor antagonists inhibit the development of physical dependence and tolerance (Trujillo, 2000). The NMDA receptor antagonists memantine (Ribeiro Do Couto et al, 2004) and MK-801 (Tzschentke and Schmidt, 1995) are capable of preventing the acquisition of morphine-induced conditioned place-preference, suggesting that the glutamatergic system can modulate opiate reward.…”

Section: Glutamate and Neuroplasticity -Implications For The Toxicitymentioning

confidence: 99%

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

194

136

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Are NMDA receptors involved in opiate-induced neural and behavioral plasticity?

Cited by 126 publications

References 166 publications

Glycyl-Glutamine, an Endogenous β-Endorphin-Derived Peptide, Inhibits Morphine-Induced Conditioned Place Preference, Tolerance, Dependence, and Withdrawal

Glycyl-Glutamine, an Endogenous β-Endorphin-Derived Peptide, Inhibits Morphine-Induced Conditioned Place Preference, Tolerance, Dependence, and Withdrawal

(–)-(1R,2R)-3-(3-Dimethylamino-1-ethyl-2-methyl-propyl)-phenol Hydrochloride (Tapentadol HCl): a Novel μ-Opioid Receptor Agonist/Norepinephrine Reuptake Inhibitor with Broad-Spectrum Analgesic Properties

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

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