Orphanin FQ/nociceptin blocks methamphetamine place preference in rats

Zhao, Rongjie; Woo, Ran-Sook; Jeong, Min-Suk; Shin, Byoung‐Soo; Kim, Dong-Goo; Kim, Kee-Won

doi:10.1097/00001756-200312190-00019

Cited by 48 publications

(39 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…These results are consistent with previous studies showing that exogenous N/OFQ administration suppresses the acquisition or expression of drug-induced CPP (Ciccocioppo et al, 1999(Ciccocioppo et al, , 2000Murphy et al, 1999;Kotlinska et al, 2003;Kuzmin et al, 2003;Zhao et al, 2003;Sakoori and Murphy, 2004).…”

Section: Role Of Endogenous N/ofq In Balancing Hedonic Statesupporting

confidence: 93%

Endogenous Nociceptin (Orphanin FQ) Suppresses Basal Hedonic State and Acute Reward Responses to Methamphetamine and Ethanol, but Facilitates Chronic Responses

Sakoori

Murphy

2007

Neuropsychopharmacol

View full text Add to dashboard Cite

The opioid peptide nociceptin (orphanin FQ) suppresses drug reward, drug self-administration, and impedes some of the processes believed to underlie the transition to addiction. As virtually all previous studies have used administration of nociceptin receptor agonists to evaluate the role of nociceptin on addiction-like behavior, the current study used a pharmacological (nociceptin receptor antagonist) and genetic (nociceptin receptor knockout mice) approach to elucidate the role of endogenous nociceptin. The nociceptin receptor antagonist UFP-101 induced a modest place preference, and enhanced the conditioned place preference induced by methamphetamine. In agreement with this, nociceptin receptor knockout mice had slightly enhanced methamphetamine and ethanol conditioned place preferences compared to wild-type mice. This effect did not appear to depend on differences in learning ability, as nociceptin receptor knockout mice had slightly weaker-conditioned place aversions to lithium chloride, the k-opioid receptor agonist, U50488H, and the general opiate antagonist, naloxone. The development of behavioral sensitization to methamphetamine was lower in nociceptin receptor knockout mice, and attenuated by UFP-101 administration to wild-type mice. Additionally, ethanol consumption and preference in a two-bottle choice test was lower in nociceptin receptor knockout mice, though ethanol-stimulated locomotion was stronger. Whereas the rewarding effect of methamphetamine and ethanol following chronic treatment, as measured by place conditioning, strengthened in wild-type mice, this effect was absent in nociceptin receptor knockout mice. These results suggest that endogenous N/OFQ suppresses basal and drug-stimulated increases in hedonic state, and plays either a permissive or facilitatory role in the development of addiction.

show abstract

Section: Role Of Endogenous N/ofq In Balancing Hedonic Statesupporting

confidence: 93%

Endogenous Nociceptin (Orphanin FQ) Suppresses Basal Hedonic State and Acute Reward Responses to Methamphetamine and Ethanol, but Facilitates Chronic Responses

Sakoori

Murphy

2007

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…2. NOP receptor agonists block contextual drug associations (i.e., CPP) of every drug tested, including morphine, cocaine, amphetamine, and alcohol (Ciccocioppo et al, 2000;Kotlinska et al, 2002Kotlinska et al, , 2003Zhao et al, 2003;Sakoori and Murphy, 2004). This is consistent with a NOP receptor agonist-induced decrease in extracellular dopamine in the NAc (Murphy et al, 1996;Vazquez-DeRose et al, 2013).…”

Section: Future Directions and New Toolsmentioning

confidence: 68%

“…Initial studies demonstrated that N/OFQ is neither rewarding nor aversive (Devine et al, 1996). In fact, intracerebroventricularly administered N/OFQ can block morphine CPP and CPP induced by cocaine, alcohol, and methamphetamine (Ciccocioppo et al, 2000;Kotlinska et al, 2002Kotlinska et al, , 2003Zhao et al, 2003;Sakoori and Murphy, 2004). N/OFQ also blocks self-administration of alcohol (Ciccocioppo et al, 2004).…”

Section: Biologic Actions Of Nociceptin Opioid Peptide Receptorsmentioning

confidence: 99%

Nociceptin/Orphanin FQ Receptor Structure, Signaling, Ligands, Functions, and Interactions with Opioid Systems

et al. 2016

View full text Add to dashboard Cite

The NOP receptor (nociceptin/orphanin FQ opioid peptide receptor) is the most recently discovered member of the opioid receptor family and, together with its endogenous ligand, N/OFQ, make up the fourth members of the opioid receptor and opioid peptide family. Because of its more recent discovery, an understanding of the cellular and behavioral actions induced by NOP receptor activation are less well developed than for the other members of the opioid receptor family. All of these factors are important because NOP receptor activation has a clear modulatory role on mu opioid receptor-mediated actions and thereby affects opioid analgesia, tolerance development, and reward. In addition to opioid modulatory actions, NOP receptor activation has important effects on motor function and other physiologic processes. This review discusses how NOP pharmacology intersects, contrasts, and interacts with the mu opioid receptor in terms of tertiary structure and mechanism of receptor activation; location of receptors in the central nervous system; mechanisms of desensitization and downregulation; cellular actions; intracellular signal transduction pathways; and behavioral actions with respect to analgesia, tolerance, dependence, and reward. This is followed by a discussion of the agonists and antagonists that have most contributed to our current knowledge. Because NOP receptors are highly expressed in brain and spinal cord and NOP receptor activation sometimes synergizes with mu receptor-mediated actions and sometimes opposes them, an understanding of NOP receptor pharmacology in the context of these interactions with the opioid receptors will be crucial to the development of novel therapeutics that engage the NOP receptor

show abstract

“…]nociceptin-NH 2 (UFP-101), suggesting that the buprenorphine-induced reduction in alcohol consumption is caused by activation of NOP receptors (Ciccocioppo et al, 2007). An NOP-mediated reduction in CPP and self-administration of a variety of abused drugs by N/OFQ is already well documented (Murphy et al, 1999;Kotliń ska et al, 2002;Ciccocioppo et al, 2003;Zhao et al, 2003). Therefore, it is possible that increasing the NOP agonist efficacy in buprenorphine, or other opioid ligands, may produce an effective nonaddicting analgesic and may be more efficacious than buprenorphine for drug abuse pharmacotherapy.…”

Section: Discussionmentioning

confidence: 99%

“…N/OFQ, through NOP-receptor activation, has been shown to have antiopiate properties in the brain (Meunier et al, 1995;Reinscheid et al, 1995) and is able to block the reward induced by morphine (Murphy et al, 1999), cocaine (Kotliń ska et al, 2002;Sakoori and Murphy, 2004), ethanol (Ciccocioppo et al, 1999;Kuzmin et al, 2003), and methamphetamine (Zhao et al, 2003). N/OFQ, when administered intracerebroventricularly, also has been shown to block development of tolerance to morphine (Lutfy et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

The First Universal Opioid Ligand, (2S)-2-[(5R,6R,7R,14S)-N-cyclopropylmethyl-4,5-epoxy-6,14-ethano-3-hydroxy-6-methoxymorphinan-7-yl]-3,3-dimethylpentan-2-ol (BU08028): Characterization of the In Vitro Profile and In Vivo Behavioral Effects in Mouse Models of Acute Pain and Cocaine-Induced Reward

Khroyan¹,

Polgar²,

Cami‐Kobeci³

et al. 2010

J Pharmacol Exp Ther

View full text Add to dashboard Cite

Certain behavioral features of buprenorphine, including a bellshaped curve for antinociception and attenuation of alcohol consumption, are thought to be mediated by activation of nociceptin/orphanin FQ peptide (NOP) receptors, despite moderate affinity and low efficacy at NOP receptors. We hypothesized that ligands with buprenorphine's physical properties, but possessing increased NOP receptor affinity and efficacy, would improve the profile as a drug abuse medication and reduce addiction liability. Using this strategy, we designed several compounds with universally high affinity, i.e., less than 10 nM at , ␦, , and NOP receptors. Among these, (2S)-2-[(5R,6R,7R,14S)-N-cyclopropylmethyl-4,5-epoxy-6,14-ethano-3-hydroxy-6-methoxymorphinan-7-yl]-3,3-dimethylpentan-2-ol (BU08028) has high affinity at all opioid receptors and increased NOP receptor efficacy in vitro in the [35 S]GTP␥S binding assay, however, while still being a partial agonist. In vivo, BU08028 was evaluated in an acute thermal antinociception assay, for its ability to induce conditioned place preference (CPP), and for its effect on cocaine-induced CPP. BU08028 is a very potent long-lasting analgesic. It produces an increase in locomotor activity and a significant CPP. As a pretreatment to cocaine, BU08028 does not alter cocaine CPP but causes a further increase in cocaine-induced locomotor activity. The analgesic, rewarding, and stimulant effects are probably caused by receptor stimulation. It is likely that with BU08028, a partial agonist at both NOP and receptors, -mediated activity overpowers NOPmediated effects. Thus, it is possible that a different buprenorphine analog that is a universal high-affinity opioid ligand but with "full agonist" activity at NOP may counteract traditional opioidmediated effects such as antinociception and reward.

show abstract

Orphanin FQ/nociceptin blocks methamphetamine place preference in rats

Cited by 48 publications

References 19 publications

Endogenous Nociceptin (Orphanin FQ) Suppresses Basal Hedonic State and Acute Reward Responses to Methamphetamine and Ethanol, but Facilitates Chronic Responses

Endogenous Nociceptin (Orphanin FQ) Suppresses Basal Hedonic State and Acute Reward Responses to Methamphetamine and Ethanol, but Facilitates Chronic Responses

Nociceptin/Orphanin FQ Receptor Structure, Signaling, Ligands, Functions, and Interactions with Opioid Systems

The First Universal Opioid Ligand, (2S)-2-[(5R,6R,7R,14S)-N-cyclopropylmethyl-4,5-epoxy-6,14-ethano-3-hydroxy-6-methoxymorphinan-7-yl]-3,3-dimethylpentan-2-ol (BU08028): Characterization of the In Vitro Profile and In Vivo Behavioral Effects in Mouse Models of Acute Pain and Cocaine-Induced Reward

Contact Info

Product

Resources

About