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Crombag H.S., Grimm J.W., and Shaham Y. Effect of dopamine receptor antagonists on renewal of cocaine seeking by reexposure to drug-associated contextual cues. Neuropsychopharmacology 27 (2002) 1006-1015
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Bassareo V, De Luca MA, Di Chiara G: Differential impact of pavlovian drug conditioned stimuli on in vivo dopamine transmission in the rat accumbens shell and core and in the prefrontal cortex. Psychopharmacology (Berl) 2006, in press. This study investigates, by microdialysis, the response of extracellular DA in three different terminal areas - the NAc shell and core and medial PFC - to a salient complex olfactory-visual contextual stimulus (a perforated box filled up with a snack food) conditioned to systemic morphine or nicotine. Similar effects were observed with each drug. After three drug-stimulus associations, box presentation elicited strong incentive responses towards the box and increased DA in the shell and PFC, but not in the core, in conditioned, but not in unconditioned and pseudoconditioned, groups. Pre-exposure to the drug conditioned stimuli potentiated drug-induced increase of DA in the shell but not in the core. These observations show that drug conditioned stimuli differentially affect accumbens DA when compared with food conditioned stimuli. Thus, as reported by [21,24] and by [23], food conditioned stimuli stimulate DA efflux in the NAc core and PFC, but not in the NAc shell.
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Di Chiara G. A motivational learning hypothesis of the role of mesolimbic dopamine in compulsive drug use. J Psychopharmacol 12 (1998) 54-67
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Di Chiara, G.1
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••], shows that intra-shell infusion of D1 receptor antagonists impairs acquisition but not expression of drug-conditioned place preference. It is suggested that drugs, by activating DA transmission in the shell, induce an incentive arousal state that elicits hedonia and facilitates incentive learning.
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••], shows that intra-shell infusion of D1 receptor antagonists impairs acquisition but not expression of drug-conditioned place preference. It is suggested that drugs, by activating DA transmission in the shell, induce an incentive arousal state that elicits hedonia and facilitates incentive learning.
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Bassareo V., De Luca M.A., Aresu M., Aste A., AriuT, and Di Chiara G. Differential adaptive properties of accumbens shell dopamine responses to ethanol as a drug and as a motivational stimulus. Eur J Neurosci 17 (2003) 1465-1472
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On the basis of neuropsychological and brain imaging studies, the author suggests that addiction is the product of an imbalance between two separate, but interacting, neural systems that control decision making: an impulsive amygdala system for signaling pain or pleasure of immediate prospects, and a reflective PFC system for signaling pain or pleasure of future prospects. After an individual learns social rules, the reflective system controls the impulsive system via several mechanisms. However, this control is not absolute; hyperactivity within the impulsive system can override the reflective system. It is proposed that drugs can trigger 'bottom-up' involuntary signals originating from the amygdala that modulate, bias or even hijack the goal-driven cognitive resources that are needed for the normal operation of the reflective system and for exercising the willpower to resist drugs.
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Bechara A. Decision making, impulse control and loss of willpower to resist drugs: a neurocognitive perspective. Nat Neurosci 8 (2005) 1458-1463. On the basis of neuropsychological and brain imaging studies, the author suggests that addiction is the product of an imbalance between two separate, but interacting, neural systems that control decision making: an impulsive amygdala system for signaling pain or pleasure of immediate prospects, and a reflective PFC system for signaling pain or pleasure of future prospects. After an individual learns social rules, the reflective system controls the impulsive system via several mechanisms. However, this control is not absolute; hyperactivity within the impulsive system can override the reflective system. It is proposed that drugs can trigger 'bottom-up' involuntary signals originating from the amygdala that modulate, bias or even hijack the goal-driven cognitive resources that are needed for the normal operation of the reflective system and for exercising the willpower to resist drugs.
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Bechara, A.1
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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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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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Rothman R.B., Gorelick D.A., Baumann M.H., Guo X.Y., Herning R.I., Pickworth W.B., Gendron T.M., Koeppl B., Thomson III L.E., and Henningfield J.E. Lack of evidence for context-dependent cocaine-induced sensitization in humans: preliminary studies. Pharmacol Biochem Behav 49 (1994) 583-588
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Charles P.O. Drug addiction and drug abuse. In: Hardman J.G., Gilman A.G., and Limbird L.E. (Eds). Goodman & Gilman's - The Pharmacological Basis of Therapeutics (2001), McGraw-Hill, New York
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Charles, P.O.1
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Reid M.S., Ciplet D., O'Leary S., Branchey M., Buydens-Branchey L., and Angrist B. Sensitization to the psychosis-inducing effects of cocaine compared with measures of cocaine craving and cue reactivity. Am J Addict 13 (2004) 305-315
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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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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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Int Rev Neurobiol
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Neurobiology of relapse to heroin and cocaine seeking: an update and clinical implications
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The authors provide a review of recent data on the neurobiology of relapse. An important point they make is the discrepancy between results obtained by total DA inactivation and those obtained by lesion or local manipulation of DA transmission by infusion of specific DA receptor agonists and antagonists.
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Bossert J.M., Ghitza U.E., Lu L., Epstein D.S., and Shaham Y. Neurobiology of relapse to heroin and cocaine seeking: an update and clinical implications. Eur J Pharmacol 526 (2005) 36-50. The authors provide a review of recent data on the neurobiology of relapse. An important point they make is the discrepancy between results obtained by total DA inactivation and those obtained by lesion or local manipulation of DA transmission by infusion of specific DA receptor agonists and antagonists.
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Eur J Pharmacol
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Anatomy and pharmacology of cocaine priming-induced reinstatement of drug seeking
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The authors review the controversial issue of the role of specific DA terminal areas in reinstatement induced by cocaine priming, and provide important evidence for a role for NAc shell DA in cocaine priming.
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Schmidt H.D., Anderson S.M., Famous K.R., Kumaresan V., and Pierce R.C. Anatomy and pharmacology of cocaine priming-induced reinstatement of drug seeking. Eur J Pharmacol 526 (2005) 65-76. The authors review the controversial issue of the role of specific DA terminal areas in reinstatement induced by cocaine priming, and provide important evidence for a role for NAc shell DA in cocaine priming.
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Eur J Pharmacol
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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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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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Weiss F., Maldonado-Vlaar C.S., Parsons L.H., Kerr T.M., Smith D.L., and Ben-Shahar O. Control of cocaine-seeking behavior by drug-associated stimuli in rats: effects on recovery of extinguished operant-responding and extracellular dopamine levels in amygdala and nucleus accumbens. Proc Natl Acad Sci USA 97 (2000) 4321-4326
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Fuchs R.A., Branham R.K., and See R.E. Different neural substrates mediate cocaine seeking after abstinence versus extinction training: a critical role for the dorsolateral caudate-putamen. J Neurosci 26 (2006) 3584-3588
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Ito R., Dalley J.W., Robbins T.W., and Everitt B.J. Dopamine release in the dorsal striatum during cocaine-seeking behavior under the control of a drug-associated cue. J Neurosci 22 (2002) 6247-6253
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