Reactivation of cocaine conditioned place preference induced by stress is reversed by cholecystokinin-B receptors antagonist in rats

Lü, Lin; Zhang, Ben; Liu, Zhiyuan; Zhang, Zhanyin

doi:10.1016/s0006-8993(02)03359-0

Cited by 62 publications

(30 citation statements)

References 59 publications

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“…The rats then received another CPP test on day 24 (extinction); after a 2-week period of extinction training, most rats did not present conditioned preference for the drug-paired side as described previously (Lu et al 2002;Mueller and Stewart 2000).…”

Section: Intracerebral Cannulae Implantationmentioning

confidence: 99%

Region-specific effects of brain corticotropin-releasing factor receptor type 1 blockade on footshock-stress- or drug-priming-induced reinstatement of morphine conditioned place preference in rats

Wang

Fang²,

et al. 2005

Psychopharmacology

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Section: Intracerebral Cannulae Implantationmentioning

confidence: 99%

Region-specific effects of brain corticotropin-releasing factor receptor type 1 blockade on footshock-stress- or drug-priming-induced reinstatement of morphine conditioned place preference in rats

Wang

Fang²,

et al. 2005

Psychopharmacology

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120

101

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“…Footshock leads to reinstatement of previously extinguished operant responding for cocaine (Ahmed and Koob, 1997; Erb et al, 1996), heroin (Shaham and Stewart, 1995; Shaham, 1996; Shaham et al, 1996), nicotine (Buczek et al, 1999) and alcohol (Le et al, 1998) self-administration. Footshock stress has also been shown to reactivate extinguished conditioned place preference (CPP) behavior for both cocaine and morphine conditioned reward (Lu et al, 2002; Wang et al, 2006; Wang et al, 2001). In addition to footshock, stressors such as restraint, tail pinch, and forced swim stress have also been shown to reactivate drug CPP (Kreibich and Blendy, 2004; Leao et al, 2009; Sanchez et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Molecular and genetic substrates linking stress and addiction

2010

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Drug addiction is one of the top three health concerns in the United States in terms of economic and health care costs. Despite this, there are very few effective treatment options available. Therefore, understanding the causes and molecular mechanisms underlying the transition from casual drug use to compulsive drug addiction could aid in the development of treatment options. Studies in humans and animal models indicate that stress can lead to both vulnerability to develop addiction, as well as increase drug taking and relapse in addicted individuals. Exposure to stress or drugs of abuse results in long-term adaptations in the brain that are likely to involve persistent alterations in gene expression or activation of transcription factors, such as the cAMP Response Element Binding protein, CREB. The signaling pathways controlled by CREB have been strongly implicated in drug addiction and stress. Many potential CREB target genes have been identified based on the presence of a CRE element in promoter DNA sequences. These include, but are not limited to CRF, BDNF, and dynorphin. These genes have been associated with initiation or reinstatement of drug reward and are altered in one direction or the other following stress. While many reviews have examined the interactions between stress and addiction, the goal of this review is to focus on specific molecules that play key roles in both stress and addiction and are therefore posed to mediate the interaction between the two. Focus on these molecules could provide us with new targets for pharmacological treatments for addiction.

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“…Importantly, several behavioral studies indicate that memory for CPPs is subject to extinction, as nonrewarded exposure to environmental contexts previously paired with rewarding drug treatments reduces subsequent CPP behavior (Bardo et al 1986;Calcagnetti and Schecter 1993;Mueller and Stewart 2000;Parker and McDonald 2000;Itzhak and Martin 2001;Lu et al 2002). Although extinction of CPP behavior has been demonstrated in several studies, the neurobiological basis of extinction in this task has not been extensively investigated.…”

mentioning

confidence: 99%

Facilitation of Memory for Extinction of Drug-Induced Conditioned Reward: Role of Amygdala and Acetylcholine

Schroeder¹,

Packard²

2004

Learn. Mem.

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These experiments examined the effects of posttrial peripheral and intra-amygdala injections of the cholinergic muscarinic receptor agonist oxotremorine on memory consolidation underlying extinction of amphetamine conditioned place preference (CPP) behavior. Male Long-Evans rats were initially trained and tested for an amphetamine (2 mg/kg) CPP. Rats were subsequently given limited extinction training, followed by immediate posttrial peripheral or intrabasolateral amygdala injections of oxotremorine. A second CPP test was then administered, and the amount of time spent in the previously amphetamine-paired and saline-paired apparatus compartments was recorded. Peripheral (0.07 or 0.01 mg/kg) or intra-amygdala (10 g/0.5µL) postextinction trial injections of oxotremorine facilitated CPP extinction. Oxotremorine injections that were delayed 2 h posttrial training did not enhance CPP extinction, indicating a time-dependent effect of the drug on memory consolidation processes. The findings indicate that memory consolidation for extinction of approach behavior to environmental stimuli previously paired with drug reward can be facilitated by posttrial peripheral or intrabasolateral amygdala administration of a cholinergic agonist.In the conditioned place preference (CPP) paradigm, the rewarding properties of a treatment are assessed by measuring approach behavior to environmental cues paired previously with the affective consequences of treatment administration. As numerous drugs with abuse potential in humans reliably induce a CPP in experimental animals, this task has been used extensively to investigate the neurobiological bases of drug reward (for reviews, see Carr et al. 1989;Tzschentke 1998). Following pairings of a drug treatment with a specific environmental context, the expression of a CPP is assessed on a treatment-free test day. Therefore, CPP behavior ultimately involves acquisition, consolidation, and retrieval of stimulus-reward memory for an association between environmental stimuli and the affective state produced by a treatment (White and Carr 1985;Hsu et al. 2002).Extinction of memories mediating the control of approach behavior to environmental cues that have been associated with rewarding drug treatments represents a potentially significant therapeutic approach to human drug addiction. Importantly, several behavioral studies indicate that memory for CPPs is subject to extinction, as nonrewarded exposure to environmental contexts previously paired with rewarding drug treatments reduces subsequent CPP behavior (Bardo et al. 1986; Calcagnetti and Schecter 1993;Mueller and Stewart 2000;Parker and McDonald 2000;Itzhak and Martin 2001;Lu et al. 2002). Although extinction of CPP behavior has been demonstrated in several studies, the neurobiological basis of extinction in this task has not been extensively investigated. Several lines of evidence indicate that extinction involves new learning, rather than simple forgetting or erasure of original learning (see Bouton 1993;Rescorla 2001). Therefore, we have re...

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Reactivation of cocaine conditioned place preference induced by stress is reversed by cholecystokinin-B receptors antagonist in rats

Cited by 62 publications

References 59 publications

Region-specific effects of brain corticotropin-releasing factor receptor type 1 blockade on footshock-stress- or drug-priming-induced reinstatement of morphine conditioned place preference in rats

Region-specific effects of brain corticotropin-releasing factor receptor type 1 blockade on footshock-stress- or drug-priming-induced reinstatement of morphine conditioned place preference in rats

Molecular and genetic substrates linking stress and addiction

Facilitation of Memory for Extinction of Drug-Induced Conditioned Reward: Role of Amygdala and Acetylcholine

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