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Volumn 7, Issue 1, 2007, Pages 69-76

Reward system and addiction: what dopamine does and doesn't do (DOI:10.1016/j.coph.2006.11.003);Reward system and addiction: what dopamine does and doesn't do

Author keywords

[No Author keywords available]

Indexed keywords

COCAINE; DOPAMINE; DOPAMINE 2 RECEPTOR; G PROTEIN COUPLED RECEPTOR; PSYCHOSTIMULANT AGENT;

EID: 33846903376     PISSN: 14714892     EISSN: None     Source Type: Journal    
DOI: 10.1016/j.coph.2007.02.001     Document Type: Erratum
Times cited : (425)

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    • Everitt B.J., and Robbins T.W. Neural systems of reinforcement for drug addiction: from actions to habits to compulsion. Nat Neurosci 8 (2005) 1481-1489. The authors view drug addiction as a process involving a transition from different modalities of responding that depend upon interactions between Pavlovian and instrumental learning processes. They hypothesize that the change from voluntary drug use to more habitual and compulsive drug use represents a transition from prefrontal cortical control to striatal control over drug-seeking and drug-taking behaviour, as well as a progression in dopaminergic innervation from ventral to more dorsal domains of the striatum. These neural transitions might themselves depend upon the neuroplasticity in both cortical and striatal structures that is induced by chronic self-administration of drugs.
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    • Melis M., Spiga S., and Diana M. The dopamine hypothesis of drug addiction: hypodopaminergic state. Int Rev Neurobiol 63 (2005) 101-154. This review provides a view of dependence in terms of neuroadaptive changes of the DA system to chronic drug exposure, resulting in the induction of processes opposite to the DA-stimulant properties of addictive drugs. As a result of this process, drug withdrawal results in depression of DA transmission and firing of DA neurons that exceeds the duration of the physical signs of abstinence, and is attributed the role of promoting drug seeking. This hypothesis is a natural development of the theory by Koob et al. [63]. Indeed, given the evidence for a role of DA in intracranial self-stimulation, the observation made by Koob et al. [63] that abstinence from chronic drug exposure raises the threshold for intracranial self-stimulation is well explained as a consequence of the reduction in DA transmission induced by chronic drug exposure. Curiously, however, Koob et al. [63] are apparently reluctant to make this connection.
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    • See R. Neural substrates of cocaine-cue associations that trigger relapse. Eur J Pharmacol 526 (2005) 140-146. This paper reviews studies from the authors' laboratory and from others on the role of the basolateral amygdala in learning cue-drug associations relevant for relapse. Reversible pharmacological inactivation of the basolateral complex of the amygdala just prior to acquisition of cocaine-cue associations blocks the ability of cocaine-paired stimuli to elicit conditioned-cued reinstatement. This learning process is mediated in part by muscarinic acetylcholine and dopaminergic inputs, as intra-amygdala infusion of selective receptor antagonists at the time of acquisition affects reinstatement. Disruption of neural activity within the basolateral complex of the amygdala at the time of consolidation (just after cocaine-cue pairings) also disrupts reinstatement. These results reveal the importance of the amygdala in the acquisition, consolidation and expression of drug-stimulus learning that drives relapse to drug-seeking behavior.
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