Disruption of nicotine conditioning
by dopamine D(3) receptor ligands
by
Le Foll B, Schwartz JC, Sokoloff P
Mol Psychiatry 2003 Feb;8(2):225-30

ABSTRACT

Tobacco smoking is the first cause of preventable death in modern countries. Nicotine replacement therapy or sustained release bupropion helps smoking cessation, but relapse rates are still very high. Nicotine, like other drugs of abuse, activates the dopamine mesolimbic system, which originates in the ventral tegmental area and projects notably to the nucleus accumbens. Situations or environmental stimuli previously associated with cigarette smoking, for example, smell of cigarette smoke, can elicit craving in abstinent smokers and promote relapse. Reducing the effects of nicotine-associated cues might therefore have potential therapeutic utility for smoking cessation. Such an approach has been validated for cocaine in animals, by using the dopamine D(3) receptor-selective partial agonist BP 897, which inhibits cocaine cue-induced drug-seeking behavior. Here we show that rats repeatedly injected with nicotine in a particular environment develop nicotine-conditioned locomotor responses, accompanied by an increase in D(3) receptor expression in the nucleus accumbens. This conditioned behavior was inhibited by BP 897 or a selective D(3) receptor antagonist, suggesting that antagonizing dopamine selectively at the D(3) receptor disrupts nicotine-conditioned effects and might represent a novel therapeutic approach for smoking cessation

Nicotine
Tobacco
Smoking
Cotinine
Selegiline
Dopamine
Cigarettes
Free-base nicotine
Nicotine : structure
Parkinson's disease
Smoking and MAO-A
Smoking and MAO-B
Nicotine neuroprotection
Nicotine, dopamine and reward
Muscarinic + nicotinic receptors
Bupropion and nicotinic receptors
Non-nicotinic drugs for tobacco addicts
Tranylcypromine (Parnate) and nicotine
Bupropion (Zyban) for cigarette smokers
Quitting smoking: the role of antidepressants
Nicotine self-administration and increased reward-sensitivity

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