Differential neurochemical and behavioral adaptation to cocaine after response contingent and noncontingent exposure in the rat

Lecca, Daniele; Cacciapaglia, Fabio; Valentini, Valentina; Acquas, Elio; Chiara, G. Di

doi:10.1007/s00213-006-0496-y

Cited by 110 publications

(113 citation statements)

References 46 publications

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“…Indeed, neurobiological correlates of reward (eg neurotransmitter release in the basal ganglia) are increased after response-contingent drug infusions by a far greater magnitude than by response non-contingent drug infusions (Wilson et al, 1994;Mark et al, 1999;Kimmel et al, 2005;Lecca et al, 2007). In addition, different gene expression, neurochemical, stress system, and behavioral adaptations occur in response to volitional vs nonvolitional drug consumption (Stefanski et al, 1999;Jacobs et al, 2005).…”

Section: Reward-enhancing and Reinforcing Effects Of Nicotine Requirementioning

confidence: 99%

NMDA Receptors Regulate Nicotine-Enhanced Brain Reward Function and Intravenous Nicotine Self-Administration: Role of the Ventral Tegmental Area and Central Nucleus of the Amygdala

Kenny

Chartoff

Roberto

et al. 2008

Neuropsychopharmacol

132

134

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Nicotine is considered an important component of tobacco responsible for the smoking habit in humans. Nicotine increases glutamatemediated transmission throughout brain reward circuitries. This action of nicotine could potentially contribute to its intrinsic rewarding and reward-enhancing properties, which motivate consumption of the drug. Here we show that the competitive N-methyl-D-aspartate (NMDA) receptor antagonist LY235959 (0.5-2.5 mg per kg) abolished nicotine-enhanced brain reward function, reflected in blockade of the lowering of intracranial self-stimulation (ICSS) thresholds usually observed after experimenter-administered (0.25 mg per kg) or intravenously self-administered (0.03 mg per kg per infusion) nicotine injections. The highest LY235959 dose (5 mg per kg) tested reversed the hedonic valence of nicotine from positive to negative, reflected in nicotine-induced elevations of ICSS thresholds. LY235959 doses that reversed nicotine-induced lowering of ICSS thresholds also markedly decreased nicotine self-administration without altering responding for food reinforcement, whereas the a-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptor antagonist NBQX had no effects on nicotine intake. In addition, nicotine self-administration upregulated NMDA receptor subunit expression in the central nucleus of the amygdala (CeA) and ventral tegmental area (VTA), suggesting important interactions between nicotine and the NMDA receptor. Furthermore, nicotine (1 mM) increased NMDA receptor-mediated excitatory postsynaptic currents in rat CeA slices, similar to its previously described effects in the VTA. Finally, infusion of LY235959 (0.1-10 ng per side) into the CeA or VTA decreased nicotine self-administration. Taken together, these data suggest that NMDA receptors, including those in the CeA and VTA, gate the magnitude and valence of the effects of nicotine on brain reward systems, thereby regulating motivation to consume the drug.

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Section: Reward-enhancing and Reinforcing Effects Of Nicotine Requirementioning

confidence: 99%

NMDA Receptors Regulate Nicotine-Enhanced Brain Reward Function and Intravenous Nicotine Self-Administration: Role of the Ventral Tegmental Area and Central Nucleus of the Amygdala

Kenny

Chartoff

Roberto

et al. 2008

Neuropsychopharmacol

132

134

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“…The DA response to a natural reward does not generally persist over time, as the organism rapidly habituates to these stimuli after a few exposures. Conversely, the response to addictive drugs is not influenced by habituation, as each drug administration stimulates the release of DA (Bradberry et al, 2000;Di Chiara et al, 2004;Lecca et al, 2007). In addition, the DA response of addictive substances is several fold higher than that elicited by novel, naturally occurring rewards .…”

Section: Mesostriatal Acetylcholine and Reward Mediationmentioning

confidence: 99%

The Role of Acetylcholine in Cocaine Addiction

Williams

Adinoff²

2007

Neuropsychopharmacol

160

138

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Central nervous system cholinergic neurons arise from several discrete sources, project to multiple brain regions, and exert specific effects on reward, learning, and memory. These processes are critical for the development and persistence of addictive disorders. Although other neurotransmitters, including dopamine, glutamate, and serotonin, have been the primary focus of drug research to date, a growing preclinical literature reveals a critical role of acetylcholine (ACh) in the experience and progression of drug use. This review will present and integrate the findings regarding the role of ACh in drug dependence, with a primary focus on cocaine and the muscarinic ACh system. Mesostriatal ACh appears to mediate reinforcement through its effect on reward, satiation, and aversion, and chronic cocaine administration produces neuroadaptive changes in the striatum. ACh is further involved in the acquisition of conditional associations that underlie cocaine self-administration and context-dependent sensitization, the acquisition of associations in conditioned learning, and drug procurement through its effects on arousal and attention. Long-term cocaine use may induce neuronal alterations in the brain that affect the ACh system and impair executive function, possibly contributing to the disruptions in decision making that characterize this population. These primarily preclinical studies suggest that ACh exerts a myriad of effects on the addictive process and that persistent changes to the ACh system following chronic drug use may exacerbate the risk of relapse during recovery. Ultimately, ACh modulation may be a potential target for pharmacological treatment interventions in cocaine-addicted subjects. However, the complicated neurocircuitry of the cholinergic system, the multiple ACh receptor subtypes, the confluence of excitatory and inhibitory ACh inputs, and the unique properties of the striatal cholinergic interneurons suggest that a precise target of cholinergic manipulation will be required to impact substance use in the clinical population.

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“…Microdialysis studies, in addition, have shown that cocaine increases extracellular DA in the NAc even after i.v. self-administration (Di Ciano et al, 1995;Justice, 1989, 1991;Wise et al, 1995;Lecca et al, 2007a). Moreover, preferential stimulation of DA transmission in the ventral striatum by amphetamine has been demonstrated in humans by Positron Emission Tomography of [ 11 C] raclopride binding (Drevets et al,1999(Drevets et al, , 2001Leyton et al, 2002;Martinez et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…This preferential action has been initially documented by microdialysis studies in acutely experimenter-administered rats (Aragona et al, 2008;Pontieri et al, 1995) and later demonstrated in rats during acquisition of i.v. cocaine SA (Lecca et al, 2007a).…”

Section: Introductionmentioning

confidence: 99%

Impairment of acquisition of intravenous cocaine self-administration by RNA-interference of dopamine D1-receptors in the nucleus accumbens shell

et al. 2015

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Microdialysis during i.v. drug self-administration (SA) have implicated nucleus accumbens (NAc) shell DA in cocaine and heroin reinforcement. However, this correlative evidence has not been yet substantiated by experimental evidence obtained by studying the effect of selective manipulation of NAc shell DA transmission on cocaine and heroin SA. In order to investigate this issue, DA D1a receptor (D1aR) expression was impaired in the NAc shell and core by locally infusing lentiviral vectors (LV) expressing specific D1aR-siRNAs (LV-siRNAs). Control rats were infused in the same areas with LV expressing GFP. Fifteen days later, rats were trained to acquire i.v. cocaine or heroin self-administration (SA). At the end of behavioral experiments, in order to evaluate the effect of LV-siRNA on D1aR expression, rats were challenged with amphetamine and the brains were processed for immunohistochemical detection of cFos and D1aR. Control rats acquired i.v. cocaine and heroin SA. Infusion of LV-siRNAs in the medial NAc shell reduced D1aR density and the number of c-Fos positive nuclei in the NAc shell, while sparing the core, and prevented the acquisition of cocaine, but not heroin SA. In turn, LV-siRNAs infusion in the core reduced D1aR density and the number of c-Fos positive nuclei in the same area, while sparing the shell, and failed to affect acquisition of cocaine. The differential effect of LV impairment of NAc shell D1aR on cocaine and heroin SA indicates that NAc shell DA acting on D1aR specifically mediates cocaine reinforcement.

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Differential neurochemical and behavioral adaptation to cocaine after response contingent and noncontingent exposure in the rat

Abstract: Response-noncontingent cocaine administration is particularly prone, compared to response-contingent administration, to induce behavioral and biochemical sensitization.

Cited by 110 publications

References 46 publications

NMDA Receptors Regulate Nicotine-Enhanced Brain Reward Function and Intravenous Nicotine Self-Administration: Role of the Ventral Tegmental Area and Central Nucleus of the Amygdala

NMDA Receptors Regulate Nicotine-Enhanced Brain Reward Function and Intravenous Nicotine Self-Administration: Role of the Ventral Tegmental Area and Central Nucleus of the Amygdala

The Role of Acetylcholine in Cocaine Addiction

Impairment of acquisition of intravenous cocaine self-administration by RNA-interference of dopamine D1-receptors in the nucleus accumbens shell

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