d-Cycloserine facilitates extinction of a cocaine-induced conditioned place preference

Botreau, Fanny; Paolone, Giovanna; Stewart, Jane

doi:10.1016/j.bbr.2006.05.012

Cited by 148 publications

(164 citation statements)

References 27 publications

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“…The results are consistent with evidence that DCS facilitates extinction in other learning tasks, including those involving Pavlovian fear conditioning (e.g., Walker et al 2002;Ledgerwood et al 2003;Richardson et al 2004) and conditioned place preference behavior (Botreau et al 2006). During latent extinction training, the previously reinforced response (in this case an approach response in a maze runway) is not overtly performed.…”

supporting

confidence: 86%

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

Gabriele¹,

Packard²

2007

Learn. Mem.

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Adult male Long-Evans rats were trained to run in a straight-alley maze for food reward and subsequently received hippocampus-dependent latent extinction training. Immediately following latent extinction, rats received peripheral injections of the NMDA receptor partial agonist D-cycloserine (DCS, 15 mg/kg), or saline. Twenty-four hours later, rats received four extinction "probe" trials. Relative to saline controls, latencies to reach the goal box on probe trials were significantly higher in rats that had received DCS. These findings indicate that memory consolidation underlying hippocampus-dependent latent extinction, a cognitive form of learning in which the previously rewarded response is not made during extinction training, can be enhanced by NMDA-receptor agonism.Behavioral extinction is operationalized as a reduction of a previously acquired response, and this process can involve new learning (for review, see Bouton 2004). The initial acquisition of learned behavior involves multiple memory systems (for review, see Packard 2001) and we have recently expanded this view to the study of the new learning underlying behavioral extinction (Gabriele and Packard 2006). We used a task in which extinction of the same overt behavior could be achieved using either a "response" or "latent" extinction training procedure. In contrast to typical extinction training that involves performance of a previously reinforced response, during latent extinction training no overt response is made. For example, a food-rewarded approach response in a straight-alley maze can be extinguished by placing the animal in the goal box in the absence of reward (Seward and Levy 1949). Consistent with the hypothesis that multiple memory systems play a role in the learning that occurs during extinction, we observed that the learning underlying response and latent extinction of runway behavior is neuroanatomically dissociable. Specifically, neural inactivation of the hippocampus prevented latent extinction of maze runway behavior, but did not block response extinction of the same behavior (Gabriele and Packard 2006). Latent extinction is conducive to a cognitive learning process in which an expectancy (Tolman 1932) of food reward can be altered without performance of the previously acquired response (Seward and Levy 1949). According to the multiple memory systems hypothesis, the hippocampus is selectively involved in cognitive learning and memory (e.g., Hirsh 1974;Mishkin and Petri 1984), and the impairment of latent extinction produced by hippocampal inactivation is consistent with this view.Although our previous study using a reversible lesion technique implicates the hippocampus in latent extinction, the findings do not provide any information concerning the neurochemical basis of this form of cognitive learning. Various neurotransmitter systems play a role in extinction (for review, see Mason 1983) and several recent studies have focused on the role of glutamatergic neurotransmission (for review, see Davis and Myers 2002). For example, adminis...

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supporting

confidence: 86%

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

Gabriele¹,

Packard²

2007

Learn. Mem.

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“…The latter is unlikely because E 2 would have also interfered with reconsolidation of extinction and our design employed repeated and prolonged exposure to the context, which favors the formation of extinction memories (Mamiya et al 2009). Moreover, there is substantial evidence that E 2 treatment enhances memory consolidation in other learning paradigms (Packard and Teather 1997;Gresack and Frick 2006a), and emerging evidence that cognitive enhancers administered during the consolidation window can facilitate extinction of cocaine (Botreau et al 2006;Paolone et al 2009) or amphetamine CPP (Schroeder and Packard 2003). Although the mnemonic and neural mechanisms underlying E 2 -induced enhancement of extinction remain unknown, the present experiments are the first to demonstrate that E 2 facilitates extinction of cocaine seeking in female rats.…”

Section: Discussionmentioning

confidence: 58%

17β-Estradiol is necessary for extinction of cocaine seeking in female rats

et al. 2013

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Human and preclinical models of addiction demonstrate that gonadal hormones modulate acquisition of drug seeking. Little is known, however, about the effects of these hormones on extinction of drug-seeking behavior. Here, we investigated how 17b-estradiol (E 2 ) affects expression and extinction of cocaine seeking in female rats. Using a conditioned place preference (CPP) paradigm, ovariectomized rats were maintained throughout conditioning with 2 d of E 2 treatment followed by 2 d of vehicle treatment, or were injected with E 2 daily. Hormone injections were paired or explicitly unpaired with place conditioning sessions. Expression of a cocaine CPP was of equal magnitude regardless of conditioning protocol, suggesting that E 2 levels during conditioning did not affect subsequent CPP expression. During extinction, daily E 2 administration initially enhanced expression of the cocaine CPP, but resulted in significantly faster extinction compared to controls. Whereas E 2 -treated rats were extinguished within 8 d, vehicle-treated rats maintained CPP expression for more than a month, indicative of perseveration. To determine whether E 2 could rescue extinction in these rats, half were given daily E 2 treatment and half were given vehicle. E 2 -treated rats showed rapid extinction, whereas vehicle-treated rats continued to perseverate. These data demonstrate for the first time that E 2 is necessary for extinction of cocaine seeking in female rats, and that it promotes rapid extinction when administered daily. Clinically, these findings suggest that monitoring and maintaining optimal E 2 levels during exposure therapy would facilitate therapeutic interventions for female cocaine addicts.Gonadal hormones render women more susceptible than men to developing compulsive patterns of psychostimulant use. Natural fluctuations in levels of the primary ovarian hormones, estrogens and progesterone, account for this increased abuse liability. Higher levels of estrogens, and lower levels of progesterone, are associated with greater sensitivity to the euphorigenic properties of cocaine in women (Evans 2007). This increased sensitivity may contribute to why women, compared with men, start using cocaine regularly at a younger age (Chen and Kandel 2002), transition from use to abuse more quickly (McCance-Katz et al. 1999), experience greater craving in response to drug-associated cues (Robbins et al. 1999) and stress (Potenza et al. 2012;Waldrop et al. 2012), and exhibit more severe drug-seeking behavior upon relapse (Gallop et al. 2007). In contrast, more women than men remain abstinent after treatment (Weiss et al. 1997). Thus, women are both more susceptible to cocaine abuse and, paradoxically, more responsive to treatment.A substantial literature supports that estrogens mediate the enhancement of drug seeking observed in females (Febo et al. 2002;Larson et al. 2007;Segarra et al. 2010; Kerstetter and Kippin 2011), but little is known regarding the role of estrogens during treatment. Preclinically, treatment is modeled through ext...

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“…Unfortunately, most of what is known about the neural mechanisms of extinction learning was derived from studies that use aversive conditioning (e.g., footshock) or appetitive conditioning with natural rewards (e.g., food). The extinction of conditioned fear in both animals and humans [69][70][71][72][73][74][75][76][77][78][79][80] as well as a cocaine CPP [81][82][83] can be facilitated by the cognitive enhancing drug D-4-amino-3-isoxazolidone [D-cycloserine (DCS)], which is a partial agonist at the strychnine-insensitive glycine site of Nmethyl-D-aspartate (NMDA) receptors [84,85]. Nic Dhonnchadha and colleagues recently found that DCS enhances the extinction learning process and inhibits reacquisition of drug self-administration in rats trained to self-administer cocaine [86].…”

Section: The Neurobiological Substrates Of Extinction Learningmentioning

confidence: 99%

“…Facilitation of glutamatergic transmission enhances extinction of drug-seeking behavior [81,83,[186][187][188]. It is likely that additional neurotransmitter systems, including dopamine and acetylcholine, are also involved in the extinction of drug-cue/context associations [3,[189][190][191].…”

Section: Role In Extinction Learningmentioning

confidence: 99%

“…It is likely that additional neurotransmitter systems, including dopamine and acetylcholine, are also involved in the extinction of drug-cue/context associations [3,[189][190][191]. Several recent studies have shown that enhancement of cholinergic and glutamatergic transmission in the BLA facilitates the extinction of a drug-paired CPP [81,190]. Schroeder and Packard have shown that the extinction of an amphetamine CPP involves cholinergic transmission in the BLA.…”

Section: Role In Extinction Learningmentioning

confidence: 99%

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Neuroanatomical Structures Underlying the Extinction of Drug-Seeking Behavior

Cleva¹,

Gass²

2013

TOADDJ

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This review summarizes current knowledge about the neurobiological components underlying the extinction of drug-associated memories and how they may contribute to the treatment of drug addiction. Evidence suggests that extinction learning is not the forgetting, or unlearning, of the associations between external stimuli and drug effects, but that new reinforcer expectancies are necessary for extinction of drug-seeking behavior to take place. Several theories suggest that addiction is a disorder of learning and memory, and recent evidence indicates that the brain circuits, neurotransmitters, and signal transduction mechanisms that underlie drug addiction are similar to those that mediate learning and memory processes. According to these theories, drug addiction results from repeated drug use and the formation of lasting associations between a drug's effects, withdrawal symptoms, and the environmental cues and contexts within which they are experienced. Unfortunately, standard behavioral modification techniques, such as cue exposure therapy, have shown only moderate efficacy in reducing and/or extinguishing the salience of drug-associated cues and contexts. Therefore, a greater understanding of the neurobiological mechanisms involved in the extinction of drug-related memories could provide novel therapeutic interventions for the treatment of drug addiction.

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d-Cycloserine facilitates extinction of a cocaine-induced conditioned place preference

Cited by 148 publications

References 27 publications

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

D-Cycloserine enhances memory consolidation of hippocampus-dependent latent extinction

17β-Estradiol is necessary for extinction of cocaine seeking in female rats

Neuroanatomical Structures Underlying the Extinction of Drug-Seeking Behavior

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