The mesolimbic dopaminergic system is implicated in the reinforcing effects of nicotine

Corrigall, William A.; Franklin, Keith B.J.; Coen, Kathleen M.; Clarke, Paul B. S.

doi:10.1007/bf02245149

Cited by 771 publications

(501 citation statements)

References 28 publications

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“…As these mechanisms would suggest, it has been shown that coadministration of methylphenidate augments nicotineinduced increases in extracellular dopamine content in the NAcc (Gerasimov et al, 2000a, b), suggesting that the interactive effects of these drugs on mesolimbic dopamine transmission underlies the behavioral interactions noted in the present study. Regarding self-administration specifically, blockade of central dopamine receptors reduces nicotine self-administration (Corrigall and Coen, 1991;Corrigall et al, 1992), whereas administration of monoamine oxidase inhibitors or the dopamine reuptake inhibitor bupropion increases nicotine self-administration (Guillem et al, 2005(Guillem et al, , 2006Rauhut et al, 2003). One caveat to this interpretation is that methylphenidate and bupropion are relatively nonselective inhibitors of the norepinephrine and dopamine transporters Han and Gu, 2006).…”

Section: Discussionmentioning

confidence: 99%

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Wooters

Neugebauer

Rush

et al. 2007

Neuropsychopharmacol

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Stimulant drugs, including D-amphetamine, cocaine, and methylphenidate, increase cigarette smoking in controlled human laboratory experiments. Although the mechanism(s) underlying this effect are unknown, it is possible that stimulants may enhance directly the abuse-related effects of nicotine. In the present study, we characterized the behavioral pharmacological interactions between methylphenidate and nicotine in the intravenous self-administration, drug discrimination, and locomotor cross-sensitization procedures. Adult male Sprague-Dawley rats were trained to respond for intravenous nicotine (0.01 or 0.03 mg/kg/infusion) or sucrose, and the acute effects of methylphenidate (1.25-10 mg/kg) were determined; in addition, separate groups of rats were treated with methylphenidate (2.5 mg/kg) or saline before 12 consecutive nicotine (0.03 mg/kg/infusion) self-administration sessions. Next, the discriminative stimulus effects of nicotine (0.03-0.3 mg/kg) and methylphenidate (1.25-10 mg/kg), alone and in combination with a low nicotine dose (0.056 mg/kg), were tested in nicotine-trained rats. Finally, the locomotor effect of repeated methylphenidate (2.5 mg/kg) was tested in rats previously treated with nicotine (0.2-0.8 mg/kg). Results indicated that acute methylphenidate increased the rate of nicotine self-administration at doses that reduced sucrose-maintained responding; furthermore, tolerance to this effect was not apparent following repeated methylphenidate. Methylphenidate, while not substituting for nicotine alone, dose-dependently enhanced the discriminative stimulus effect of a low nicotine dose. In addition, repeated nicotine exposure promoted the development of locomotor sensitization to methylphenidate. Taken together with recent clinical findings, these results suggest that methylphenidate may enhance the abuse-related behavioral effects of nicotine, perhaps increasing vulnerability to tobacco dependence.

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Section: Discussionmentioning

confidence: 99%

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Wooters

Neugebauer

Rush

et al. 2007

Neuropsychopharmacol

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“…[55][56][57] Dopamine receptors are a class of G-protein-coupled receptors with five different subtypes (D 1 -D 5 ) encoded by the genes DRD1-5. Genome-wide linkage c DSM-IV dependence was defined as a continuous score across seven ND criteria (tolerance, withdrawal, ever smoked more than meant to, difficulty quitting, great deal of time spent obtaining cigarettes, give up important social or occupational activities in order to smoke, continue smoking despite health problems caused or exacerbated by smoking) or as a categorical measure where at least three of the seven criteria were reported.…”

Section: Dopamine Receptorsmentioning

confidence: 99%

Overview of the pharmacogenomics of cigarette smoking

Tyndale

2007

Pharmacogenomics J

101

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Cigarette smoking increases the risk of numerous health problems, including cancer, cardiovascular and pulmonary disorders, making smoking the leading cause of preventable death in the world. Nicotine is primarily responsible for the highly addictive properties of cigarettes. Although the majority of smokers express a desire to quit, few are successful in doing so. Twin and family studies have indicated substantial genetic contributions to smoking behaviors. One major research focus has been to elucidate the specific genes involved; this has been accomplished primarily through genome-wide linkage analyses and candidate gene association studies. Much attention has focused on genes involved in the neurotransmitter pathways for the brain reward system and genes altering nicotine metabolism. This paper reviews the current state of knowledge for genetic factors implicated in smoking behaviors, and examines how genetic variations may affect therapeutic outcomes for drugs used to assist smoking cessation.

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“…It is well documented that nicotine stimulates dopamine (DA) release in the nucleus accumbens and striatum (Imperato et al, 1986;Damsma et al, 1989;Toth et al, 1992;Benwell and Balfour, 1994;Nisell et al, 1994a;Pontieri et al, 1996;Mirza et al, 1996;Marshall et al, 1997). This property has been related to the addictive and behavioral properties of nicotine (Benwell and Balfour, 1992;Corrigall et al, 1992;Di Chiara and Imperato, 1988).…”

Section: Introductionmentioning

confidence: 99%

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

Kim

Shim

Chung

et al. 2005

Neuropsychopharmacol

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Several studies have shown that behavioral hyperactivity induced by psychomotor stimulants is prevented by ginseng saponins. In an attempt to investigate whether the effect of ginseng saponins is through their inhibitory action on the enhanced dopaminergic transmission by psychomotor stimulants, we examined the effects of ginseng total saponin (GTS) presynaptically on nicotine-induced dopamine (DA) release in the striatum of freely moving rats using in vivo microdialysis technique and postsynaptically on the in vitro and in vivo binding of [ 3 H]raclopride to DA D 2 receptors. Also, we examined the effects of GTS on nicotine-induced locomotor hyperactivity and on nicotine-induced Fos protein expression in the nucleus accumbens and striatum. Systemic pretreatment with GTS (100 and 400 mg/kg, intraperitoneally (i.p.)) resulted in a dose-dependent inhibition of locomotor hyperactivity induced by nicotine. GTS decreased nicotine-induced DA release in the striatum in a dose-dependent manner. However, GTS had no effects on resting levels of locomotor activity and extracellular DA in the striatum. GTS inhibited the in vitro binding of [ 3 H]raclopride to rat striatal membranes with an IC 50 of 5.1471.09 mM. High doses of GTS (400 and 800 mg/kg, i.p.) resulted in decreases in the in vivo binding of [ 3 H]raclopride in the striatum. GTS decreased nicotine-induced Fos protein expression in the nucleus accumbens and striatum, reflecting the inhibition by GTS of nicotine-induced enhancement of dopaminergic transmission. The results of the present study suggest that GTS acts not only on dopaminergic neurons directly or indirectly to prevent nicotine-induced DA release but also postsynaptically by binding to DA D 2 receptors. This may explain the blocking effect of GTS on behavioral activation induced by nicotine and conceivably by other psychostimulants. Our data raise the possibility that GTS, by attenuating nicotine-induced enhancement of dopaminergic transmission, may prove to be a useful therapeutic agent for nicotine addiction and warrant further investigation on its effect on nicotine's rewarding property.

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The mesolimbic dopaminergic system is implicated in the reinforcing effects of nicotine

Cited by 771 publications

References 28 publications

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Methylphenidate Enhances the Abuse-Related Behavioral Effects of Nicotine in Rats: Intravenous Self-Administration, Drug Discrimination, and Locomotor Cross-Sensitization

Overview of the pharmacogenomics of cigarette smoking

Effect of Ginseng Saponins on Enhanced Dopaminergic Transmission and Locomotor Hyperactivity Induced by Nicotine

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