The mGluR2/3 Agonist LY379268 Induced Anti-Reinstatement Effects in Rats Exhibiting Addiction-like Behavior

Cannella, Nazzareno; Halbout, Briac; Uhrig, Stefanie; Evrard, Lionel; Corsi, Mauro; Corti, Corrado; Deroche-Gamonet, Véronique; Hansson, Anita C.; Spanagel, Rainer

doi:10.1038/npp.2013.106

Cited by 60 publications

(60 citation statements)

References 43 publications

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“…The extent of exposure to cocaine, rather than the degree of conditioning through Pavlovian pairings of CS and drug, was further shown to be a critical factor in determining the development of cocaine seeking under punishment ( Jonkman et al 2012b). Compulsive cocaine seeking in a vulnerable subgroup of rats has now been demonstrated in different strains of rats and in different laboratories , Cannella et al 2013, Chen et al 2013, Deroche-Gamonet et al 2004, Pelloux et al 2007) using three-criteria or seeking-under-threat-of-punishment procedures.…”

Section: From Habit To Compulsionmentioning

confidence: 98%

Drug Addiction: Updating Actions to Habits to Compulsions Ten Years On

Everitt

Robbins

2016

Annu. Rev. Psychol.

966

773

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A decade ago, we hypothesized that drug addiction can be viewed as a transition from voluntary, recreational drug use to compulsive drug-seeking habits, neurally underpinned by a transition from prefrontal cortical to striatal control over drug seeking and taking as well as a progression from the ventral to the dorsal striatum. Here, in the light of burgeoning, supportive evidence, we reconsider and elaborate this hypothesis, in particular the refinements in our understanding of ventral and dorsal striatal mechanisms underlying goal-directed and habitual drug seeking, the influence of drug-associated Pavlovian-conditioned stimuli on drug seeking and relapse, and evidence for impairments in top-down prefrontal cortical inhibitory control over this behavior. We further review animal and human studies that have begun to define etiological factors and individual differences in the propensity to become addicted to drugs, leading to the description of addiction endophenotypes, especially for cocaine addiction. We consider the prospect of novel treatments for addiction that promote abstinence from and relapse to drug use.

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Section: From Habit To Compulsionmentioning

confidence: 98%

Drug Addiction: Updating Actions to Habits to Compulsions Ten Years On

Everitt

Robbins

2016

Annu. Rev. Psychol.

966

773

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“…Compulsive-cocaine rats also have decreased forebrain serotonin, and depleting forebrain serotonin (or application of 5HT2C antagonists) induces compulsive behavior in rats that had only limited cocaine intake (Pelloux, Dilleen, Economidou, Theobald, & Everitt, 2012). In the prelimbic mPFC, long-term depression of mGluR2/3 is inhibited in compulsive-cocaine rats (Kasanetz et al, 2012, see also Brown, Flynn, Smith, & Dayas, 2011), and mGluR2/3 agonists decrease cocaine reinstatement (Cannella et al, 2013). In addition, alcohol-dependent rats show decreased mGluR2 levels, and restoring mGluR2 expression in the infralimbic mPFC depresses alcohol intake (Meinhardt et al, 2013).…”

Section: Molecular and Circuit Mechanisms That Promote Aversion-resismentioning

confidence: 99%

Rodent models for compulsive alcohol intake

Hopf¹,

Lesscher²

2014

Alcohol

169

176

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Continued seeking and drinking of alcohol despite adverse legal, health, economic, and societal consequences is a central hallmark of human alcohol use disorders. This compulsive drive for alcohol, defined by resistance to adverse and deleterious consequences, represents a major challenge when attempting to treat alcoholism clinically. Thus, there has long been interest in developing pre-clinical rodent models for the compulsive drug use that characterizes drug addiction. Here, we review recent studies that have attempted to model compulsive aspects of alcohol and cocaine intake in rodents, and consider technical and conceptual issues that need to be addressed when trying to recapitulate compulsive aspects of human addiction. Aversion-resistant alcohol intake has been examined by pairing intake or seeking with the bitter tastant quinine or with footshock, and exciting recent work has used these models to identify neuroadaptations in the amygdala, cortex, and striatal regions that promote compulsive intake. Thus, rodent models do seem to reflect important aspects of compulsive drives that sustain human addiction, and will likely provide critical insights into the molecular and circuit underpinnings of aversion-resistant intake as well as novel therapeutic interventions for compulsive aspects of addiction.

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“…141 Other lines of evidence support an important role for mGlu2 receptors in drug addiction as well. 97,102,146 …”

Section: Central Glutamate Activity and Alcohol Dependencementioning

confidence: 99%

Ethanol-Associated Changes in Glutamate Reward Neurocircuitry: A Minireview of Clinical and Preclinical Genetic Findings

Bell¹,

Hauser²,

McClintick³

et al. 2016

Progress in Molecular Biology and Translational Science

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Herein, we have reviewed the role of glutamate, the major excitatory neurotransmitter in the brain, in a number of neurochemical, -physiological, and -behavioral processes mediating the development of alcohol dependence. The findings discussed include results from both preclinical as well as neuroimaging and postmortem clinical studies. Expression levels for a number of glutamate-associated genes and/or proteins are modulated by alcohol abuse and dependence. These changes in expression include metabotropic receptors and ionotropic receptor subunits as well as different glutamate transporters. Moreover, these changes in gene expression parallel the pharmacologic manipulation of these same receptors and transporters. Some of these gene expression changes may have predated alcohol abuse and dependence because a number of glutamate-associated polymorphisms are related to a genetic predisposition to develop alcohol dependence. Other glutamate-associated polymorphisms are linked to age at the onset of alcohol-dependence and initial level of response/sensitivity to alcohol. Finally, findings of innate and/or ethanol-induced glutamate-associated gene expression differences/changes observed in a genetic animal model of alcoholism, the P rat, are summarized. Overall, the existing literature indicates that changes in glutamate receptors, transporters, enzymes, and scaffolding proteins are crucial for the development of alcohol dependence and there is a substantial genetic component to these effects. This indicates that continued research into the genetic underpinnings of these glutamate-associated effects will provide important novel molecular targets for treating alcohol abuse and dependence.

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The mGluR2/3 Agonist LY379268 Induced Anti-Reinstatement Effects in Rats Exhibiting Addiction-like Behavior

Cited by 60 publications

References 43 publications

Drug Addiction: Updating Actions to Habits to Compulsions Ten Years On

Drug Addiction: Updating Actions to Habits to Compulsions Ten Years On

Rodent models for compulsive alcohol intake

Ethanol-Associated Changes in Glutamate Reward Neurocircuitry: A Minireview of Clinical and Preclinical Genetic Findings

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