Parallel and interactive learning processes within the basal ganglia: Relevance for the understanding of addiction

Belin, David; Jonkman, Sietse; Dickinson, Anthony; Robbins, Trevor W.; Everitt, Barry J.

doi:10.1016/j.bbr.2008.09.027

Cited by 458 publications

(376 citation statements)

References 195 publications

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“…Drug addiction is a chronic relapsing disorder that involves progressive adaptations of cortico-striatal Nicotine modulates eCB-LTDnetworks (Yin, Ostlund, & Balleine 2008;Belin et al 2009;Belin et al 2013;Adermark et al 2016), and the data presented here suggest that the eCB system might play a role in mediating these transformations. Even though no causal relationship with behavioral transformations was assessed in this study, it is possible that nicotine-induced facilitation of eCB signaling could promote neuroadaptations and contribute to the initial conditioning and motivational effects elicited by nicotine.…”

Section: Discussionmentioning

confidence: 66%

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

et al. 2018

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The endocannabinoid (eCB) system modulates several phenomena related to addictive behaviors, and drug-induced changes in eCB signaling have been postulated to be important mediators of physiological and pathological rewardrelated synaptic plasticity. Here, we studied eCB-mediated long-term depression (eCB-LTD) in the dorsolateral striatum, a brain region critical for acquisition of habitual and automatic behavior. We report that nicotine differentially affects ex vivo eCB signaling depending on previous exposure in vivo. In the nicotine-naïve brain, nicotine facilitates eCB-signaling and LTD, whereas tolerance develops to this facilitating effect after subchronic exposure in vivo. In the end, a progressive impairment of eCB-induced LTD is established after protracted withdrawal from nicotine. Endocannabinoid-LTD is reinstated 6 months after the last drug injection, but a brief period of nicotine re-exposure is sufficient to yet again impair eCB-signaling. LTD induced by the cannabinoid 1 receptor agonist WIN55,212-2 is not affected, suggesting that nicotine modulates eCB production or release. Nicotine-induced facilitation of eCB-LTD is occluded by the dopamine D2 receptor agonist quinpirole, and by the muscarinic acetylcholine receptor antagonist scopolamine. In addition, the same compounds restore eCB-LTD during protracted withdrawal. Nicotine may thus modulate eCB-signaling by affecting dopaminergic and cholinergic neurotransmission in a long-lasting manner. Overall, the data presented here suggest that nicotine facilitates eCB-LTD in the initial phase, which putatively could promote neurophysiological and behavioral adaptations to the drug. Protracted withdrawal, however, impairs eCB-LTD, which may influence or affect the ability to maintain cessation.

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Section: Discussionmentioning

confidence: 66%

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

et al. 2018

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“…Plausibly, a similar mechanism may be observed not only for nicotine but also for different abuse substances, even if further experimental data will be necessary to support this hypothesis. Therefore, motor loworder CR-by increasing the force of that strong disabling, pervading, and recurring propensity to seek and take the substance-would contribute to the characterization of the most severe phase of addiction (i.e., drug dependence; Bcompulsive relapse^, Kalivas & O'Brien, 2008; Bloss of control of drug 2 Drug CR is sometimes associated only with less severe phases of drug addiction (following the previous terminology, drug use and drug abuse), whereas it was presumed that in the most severe phase (drug dependence), the addict does not need cues to experience his or her compulsive need to seek and take the substance (Belin, Jonkman, Dickinson, Robbins, & Everitt, 2009). Speculatively, we suggest approaching this point by considering that the salience of the cue is also a crucial point in the most severe and compulsive phase.…”

Section: Motor Cognition In Asd: Motor Anomalies Impacting On Social mentioning

confidence: 99%

The motor way: Clinical implications of understanding and shaping actions with the motor system in autism and drug addiction

Casartelli

Chiamulera

2015

Cogn Affect Behav Neurosci

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To understand others' minds is crucial for survival; however, it is quite puzzling how access to others' minds can be-to some extent-direct and not necessarily mediated by conceptual reasoning. Recent advances in neuroscience have led to hypothesize a role for motor circuits not only in controlling the elementary physical features of movement (e.g., force, direction, and amplitude), but also in understanding and shaping human behavior. The concept of Bmotor cognition^refers to these aspects, and neurophysiological, neuroimaging, and behavioral studies in human and nonhuman primates support this view. From a clinical perspective, motor cognition represents a challenge in several domains. A thorough investigation of the neural mechanisms mediating motor action/intention understanding and automatized/compulsive behaviors seems to be a promising way to tackle a range of neurodevelopmental and drug-related disorders. On the one hand, anomalies in motor cognition may have cascade effects on social functioning in individuals with autism spectrum disorder (ASD); on the other, motor cognition may help explain the pathophysiology of drug-seeking and drug-taking behaviors in the most severe phase of drug addiction (i.e., see drug dependence, motor low-order cue reactivity). This may represent a promising approach that could improve the efficacy of rehabilitative interventions. The only way to shed light on multifactorial disorders such as ASD and drug addiction is through the investigation of their multiple factors. This motor way can promote new theoretical and experimental perspectives that would help bridge the gap between the basic neuroscience approach and clinical practice.

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“…It also prevented the escalation of cocaine intake that normally occurs with prolonged cocaine access, an effect that could be blocked by disruption of miR-212 signalling using an antisense oligonucleotide. Furthermore, overexpressing miR-212 in the dorsal striatum, a neurobiological locus of control of habitual (Belin and Everitt 2008;Belin et al, 2009, Zapata et al, 2010, Murray et al, 2012 and compulsive (Jonkman et al, 2012) cocaine seeking, using a lentiviral vector reduced MeCP2 levels and decreased cocaine intake in rats with extended access to the drug (Im et al, 2010). These findings indicate that miR-212 and MeCP2 homeostatically regulate one another in the dorsal striatum and suggest that this interaction has a role in controlling compulsive cocaine intake.…”

Section: Regulation Of Cocaine Intakementioning

confidence: 81%

Addictive Drugs and Synaptic Plasticity

Negrete-Díaz¹,

Flores²,

Sihra³

et al. 2012

Addictions - From Pathophysiology to Treatment

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Parallel and interactive learning processes within the basal ganglia: Relevance for the understanding of addiction

Cited by 458 publications

References 195 publications

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

Acute and chronic modulation of striatal endocannabinoid‐mediated plasticity by nicotine

The motor way: Clinical implications of understanding and shaping actions with the motor system in autism and drug addiction

Addictive Drugs and Synaptic Plasticity

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