The effects of exogenous CCK-8 on the acquisition and expression of morphine-induced CPP

Wen, Di; Cong, Bin; Ma, Chunling; Yang, Song; Yu, Hailei; Ni, Zhiyu; Li, Shujin

doi:10.1016/j.neulet.2011.12.063

Cited by 18 publications

(13 citation statements)

References 27 publications

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“…Together with our previous results, we found that exogenous CCK-8 pretreatment significantly inhibited morphine dependence in vitro and in vivo [44]. These results show that the treatments of the CCK receptor agonist and antagonist demonstrated the same effect on morphine dependence.…”

Section: Discussionsupporting

confidence: 89%

Cholecystokinin receptor-1 mediates the inhibitory effects of exogenous cholecystokinin octapeptide on cellular morphine dependence

Wen

Meng

et al. 2012

BMC Neurosci

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BackgroundCholecystokinin octapeptide (CCK-8), the most potent endogenous anti-opioid peptide, has been shown to regulate the processes of morphine dependence. In our previous study, we found that exogenous CCK-8 attenuated naloxone induced withdrawal symptoms. To investigate the precise effect of exogenous CCK-8 and the role of cholecystokinin (CCK) 1 and/or 2 receptors in morphine dependence, a SH-SY5Y cell model was employed, in which the μ-opioid receptor, CCK1/2 receptors, and endogenous CCK are co-expressed.ResultsForty-eight hours after treating SH-SY5Y cells with morphine (10 μM), naloxone (10 μM) induced a cAMP overshoot, indicating that cellular morphine dependence had been induced. The CCK receptor and endogenous CCK were up-regulated after chronic morphine exposure. The CCK2 receptor antagonist (LY-288,513) at 1–10 μM inhibited the naloxone-precipitated cAMP overshoot, but the CCK1 receptor antagonist (L-364,718) did not. Interestingly, CCK-8 (0.1-1 μM), a strong CCK receptor agonist, dose-dependently inhibited the naloxone-precipitated cAMP overshoot in SH-SY5Y cells when co-pretreated with morphine. The L-364,718 significantly blocked the inhibitory effect of exogenous CCK-8 on the cAMP overshoot at 1–10 μM, while the LY-288,513 did not. Therefore, the CCK2 receptor appears to be necessary for low concentrations of endogenous CCK to potentiate morphine dependence in SH-SY5Y cells. An additional inhibitory effect of CCK-8 at higher concentrations appears to involve the CCK1 receptor.ConclusionsThis study reveals the difference between exogenous CCK-8 and endogenous CCK effects on the development of morphine dependence, and provides the first evidence for the participation of the CCK1 receptor in the inhibitory effects of exogenous CCK-8 on morphine dependence.

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Section: Discussionsupporting

confidence: 89%

Cholecystokinin receptor-1 mediates the inhibitory effects of exogenous cholecystokinin octapeptide on cellular morphine dependence

Wen

Meng

et al. 2012

BMC Neurosci

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“…Of note, the Large Suppressors showed a robust increase in Cck expression compared to Saline subjects. Given that Cck has been shown to attenuate the rewarding effects of opiates, the increase in Cck expression in the Large Suppressors could counteract the effects of heroin self-administration and return the subject back to homeostasis [44]. This pattern of activity may serve to ameliorate the deleterious effects that opiates have on neuronal growth and survival [27].…”

Section: Discussionmentioning

confidence: 99%

Assessment of individual differences in the rat nucleus accumbens transcriptome following taste-heroin extended access

Imperio

McFalls

Colechio

et al. 2016

Brain Research Bulletin

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Heroin addiction is a disease of chronic relapse that harms the individual through devaluation of personal responsibilities in favor of finding and using drugs. Only some recreational heroin users devolve into addiction but the basis of these individual differences is not known. We have shown in rats that avoidance of a heroin-paired taste cue reliably identifies individual animals with greater addiction-like behavior for heroin. Here rats received 5 min access to a 0.15% saccharin solution followed by the opportunity to self-administer either saline or heroin for 6 hours. Large Suppressors of the heroin-paired taste cue displayed increased drug escalation, motivation for drug, and drug loading behavior compared with Small Suppressors. Little is known about the molecular mechanisms of these individual differences in addiction-like behavior. We examined the individual differences in mRNA expression in the nucleus accumbens (NAc) of rats that were behaviorally stratified by addiction-like behavior using next-generation sequencing. We hypothesized that based on the avoidance of the drug-paired cue there will be a unique mRNA profile in the NAc. Analysis of strand-specific whole genome RNA-Seq data revealed a number of genes differentially regulated in NAc based on the suppression of the natural saccharine reward. Large Suppressors exhibited a unique mRNA prolife compared to Saline controls and Small Suppressors. Genes related to immunity, neuronal activity, and behavior were differentially expressed among the 3 groups. In total, individual differences in avoidance of a heroin-paired taste cue are associated with addiction-like behavior along with differential NAc gene expression.

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“…CCK2 receptor antagonists suppressed the acquisition and reinstatement of cocaine or morphine induced CPP [16], [17], as well as the aversive component of morphine abstinence through the CPA paradigm [18]. Interestingly, we have found that pretreatment with exogenous CCK-8 significantly inhibited the acquisition of morphine induced CPP [19]. This phenomenon suggested that the effect of exogenous CCK-8 was distinct from the role of endogenous CCK.…”

Section: Introductionmentioning

confidence: 67%

Effects of Exogenous Cholecystokinin Octapeptide on Acquisition of Naloxone Precipitated Withdrawal Induced Conditioned Place Aversion in Rats

Wen

et al. 2012

PLoS ONE

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Cholecystokinin octapeptide (CCK-8), a gut-brain peptide, regulates a variety of physiological behavioral processes. Previously, we reported that exogenous CCK-8 attenuated morphine-induced conditioned place preference, but the possible effects of CCK-8 on aversively motivated drug seeking remained unclear. To investigate the effects of endogenous and exogenous CCK on negative components of morphine withdrawal, we evaluated the effects of CCK receptor antagonists and CCK-8 on the naloxone-precipitated withdrawal-induced conditioned place aversion (CPA). The results showed that CCK2 receptor antagonist (LY-288,513, 10 µg, i.c.v.), but not CCK1 receptor antagonist (L-364,718, 10 µg, i.c.v.), inhibited the acquisition of CPA when given prior to naloxone (0.3 mg/kg) administration in morphine-dependent rats. Similarly, CCK-8 (0.1–1 µg, i.c.v.) significantly attenuated naloxone-precipitated withdrawal-induced CPA, and this inhibitory function was blocked by co-injection with L-364,718. Microinjection of L-364,718, LY-288,513 or CCK-8 to saline pretreated rats produced neither a conditioned preference nor aversion, and the induction of CPA by CCK-8 itself after morphine pretreatments was not significant. Our study identifies a different role of CCK1 and CCK2 receptors in negative affective components of morphine abstinence and an inhibitory effect of exogenous CCK-8 on naloxone-precipitated withdrawal-induced CPA via CCK1 receptor.

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The effects of exogenous CCK-8 on the acquisition and expression of morphine-induced CPP

Cited by 18 publications

References 27 publications

Cholecystokinin receptor-1 mediates the inhibitory effects of exogenous cholecystokinin octapeptide on cellular morphine dependence

Cholecystokinin receptor-1 mediates the inhibitory effects of exogenous cholecystokinin octapeptide on cellular morphine dependence

Assessment of individual differences in the rat nucleus accumbens transcriptome following taste-heroin extended access

Effects of Exogenous Cholecystokinin Octapeptide on Acquisition of Naloxone Precipitated Withdrawal Induced Conditioned Place Aversion in Rats

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