Cocaine-induced conditioned place preference: reinstatement by priming injections of cocaine after extinction

Mueller, Devin; Stewart, Jane

doi:10.1016/s0166-4328(00)00239-4

Cited by 283 publications

(235 citation statements)

References 30 publications

Supporting

Mentioning

206

Contrasting

Unclassified

Order By: Relevance

“…A similar lack of effect of other NMDA receptor antagonists was previously reported (Popik et al, 1998), where the intact place preference response was observed in rats treated with the drugs in home cages. Altogether, these data are consistent with earlier observations indicating considerable persistence of established place conditioning (Mueller and Stewart, 2000;Manzanedo et al, 2001), and showing that the drug-related neuroadaptations are highly context-dependent (Siegel and Ramos, 2002). Our data support also recent findings indicating that systemic or intra-ventral tegmental area (VTA) administration of mGluR2/3 agonist inhibits cue-induced relapse to heroin seeking in rats (Bossert et al, 2004).…”

Section: Discussionsupporting

confidence: 93%

Reinstatement of Morphine-Conditioned Reward is Blocked by Memantine

Popik

Wróbel

Bisaga

2005

Neuropsychopharmacol

View full text Add to dashboard Cite

Protection of abstinent individuals from relapse is the main goal of drug dependence treatment. Relapse is frequently precipitated by exposure to small doses of the drug of abuse or exposure to the environment that was previously associated with the drug. Mice exposed to morphine (10 mg/kg) in a unique test-box environment display a conditioned place preference for this environment. Such preference can be extinguished by subsequent pairing of physiological saline administration with the same environment. Once extinguished, the original place preference can be reinstated after a priming dose (1-2.5 mg/kg) of morphine is given. However, mice treated with 7.5 (but not 3.75) mg/kg of memantine (the glutamate/NMDA receptor antagonist) during the extinction phase were insensitive to morphine's ability to reinstate the place preference 2 days after extinction conditionings. Effect of memantine was also observed when priming dose of morphine was given 21 days after extinction conditionings. In contrast, morphine's ability to reinstate conditioned response was not affected by treatment with 10 mg/kg of chlordiazepoxide, 0.5 mg/kg of LSD-25, or 1 mg/kg of morphine given during extinction conditionings. A separate experiment demonstrated that memantine (7.5 mg/kg) treatment did not affect learning. We show for the first time that memantine treatment during extinction conditionings may abolish the ability of drug-related cues to evoke reinstatement, suggesting that this NMDA receptor antagonist can be useful in preventing relapse in opioid dependent individuals.

show abstract

Section: Discussionsupporting

confidence: 93%

Reinstatement of Morphine-Conditioned Reward is Blocked by Memantine

Popik

Wróbel

Bisaga

2005

Neuropsychopharmacol

View full text Add to dashboard Cite

show abstract

“…Previous studies have used a conditioned place preference to study relapse of drug seeking (Kreibich and Blendy 2004;Mueller and Stewart 2000). The present study, however, differs in two aspects.…”

Section: Resultsmentioning

confidence: 99%

Stress-induced reinstatement of cocaine seeking is mediated by the kappa opioid system

2008

View full text Add to dashboard Cite

Introduction-Prior activation of the kappa opioid system by repeated stress or agonist administration has been previously shown to potentiate the rewarding properties of subsequently administered cocaine. In the present study, intermittent and uncontrollable footshock, a single session of forced swim, or acute administration of the kappa agonist U50,488 (5 mg/kg) were found to reinstate place preference in mice previously conditioned with cocaine (15 mg/kg) and subsequently extinguished by repeated training sessions without drug.

show abstract

“…On this day, all mice received a prime administration, half of the conditioning dose (Mueller and Stewart, 2000) of cocaine (7.5 mg/kg, Experiments 1-3) or LiCl (75 mg/kg, Experiment 4) immediately before a 30-min test session with free access to both compartments. This test is considered to model relapse to cocaine seeking (Mueller and Stewart, 2000;Itzhak and Martin, 2002). A pilot experiment indicated that cocaine-prime administration, but not saline-prime administration, reinstates cocaine-CPP 48 h after aversive counterconditioning (Supplementary Figure S1).…”

Section: Place Conditioning Counterconditioning and Reinstatementmentioning

confidence: 99%

Counterconditioning During Reconsolidation Prevents Relapse of Cocaine Memories

Goltseker¹,

Bolotin²,

Barak

2016

Neuropsychopharmacol

View full text Add to dashboard Cite

Relapse to drug abuse is often caused by exposure to drug-associated cues that evoke craving. Therefore, disruption of the cue-drug memory can prevent relapse. Memories destabilize and become temporarily labile upon their retrieval, and re-stabilize in a process termed reconsolidation. Pharmacological disruption of reconsolidation prevents relapse in animal models, yet may evoke side effects. Therefore, behavioral procedures capable of preventing cue-induced craving and relapse are extremely valuable. Aversion therapies, in which drugpaired cues are re-associated (counterconditioned) with aversive consequences, have limited success, because the previous cue-drug memory may recover, triggering relapse. Here, we prevented the memory recovery and relapse to cocaine seeking by applying aversive counterconditioning during memory reconsolidation. Mice were trained to seek cocaine in a conditioned place preference procedure. The cocaine-associated compartment was then counterconditioned with lithium chloride (LiCl)-induced malaise, preceded by a brief exposure to the compartment (memory retrieval). Relapse was assessed in a reinstatement test. We found that aversive counterconditioning conducted shortly after memory retrieval (during reconsolidation) induced a long-lasting prevention of relapse to cocaine seeking. However, mice relapsed when counterconditioned without, before, or long after memory retrieval, or when receiving LiCl without place counterconditioning. Our findings suggest that post-retrieval aversive counterconditioning leads to relapse prevention, possibly by replacing the cue-drug with a cue-aversion memory, thereby the cue ceases to evoke craving. Moreover, we found that a similar memory replacement procedure prevented relapse of conditioned place aversion. Hence, this novel procedure can also prevent relapse of aversive memories, providing a safe approach to alter various maladaptive behaviors.

show abstract

Cocaine-induced conditioned place preference: reinstatement by priming injections of cocaine after extinction

Cited by 283 publications

References 30 publications

Reinstatement of Morphine-Conditioned Reward is Blocked by Memantine

Reinstatement of Morphine-Conditioned Reward is Blocked by Memantine

Stress-induced reinstatement of cocaine seeking is mediated by the kappa opioid system

Counterconditioning During Reconsolidation Prevents Relapse of Cocaine Memories

Contact Info

Product

Resources

About